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TOURNAL 

OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY  January  1988 


Traumatic  occupational  occlusive  arterial  disease  of  the  hands 


I ALSO:  A CASE  OF  metastatic  a community  medicine 


CARCINOMA  IN  ASSOCIATION  PROGRAM  IN  JAMAICA  FOR 

WITH  PAGET'S  DISEASE  OF  BONE  FOURTH  YEAR  MEDICAL  STUDENTS 


Louisiana 


Physicians 


Insurance  Agency, 

A Wholly  Owned  Subsidiary  of  LAMMICO 


INC. 


SPECIALLY  PRICED  PRODUCTS  OFFERED: 


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• (504)  837-3257  • 1-800-331-5777  • 

A COMMITMENT  TO  SERVE  THE  LOUISIANA  PHYSICIAN 


EDITOR 


CONWAY  S.  MAGEE,  MD 

CHIEF  EXECUTIVE  OFFICER 
DAVE  TARVER 

GENERAL  MANAGER 


RENE  ABADIE 
MANAGING  EDHOR 


BONNIE  L.  BLUNDELL 
ADVERTISING  SALES 


SISSY  SULLIVAN  HANSEN 

JOURNAL  COMMITTEE 

CONWAY  S.  MAGEE,  MD 
Chairman 

A.G.  KLEINSCHMIDT,  JR,  MD 
PAUL  F.  LARSON,  MD 
W.  CHARLES  MILLER,  MD 
EMILE  K.  VENTRE,  JR,  MD 
JAMES  W.  VILDIBILL,  JR,  MD 
Ex  officio 


EDITORIAL  BOARD 


KENNETH  B.  FARRIS,  MD 
RODNEY  C.  JUNG,  MD 
CONWAY  S.  MAGEE,  MD 
W.  CHARLES  MILLER,  MD 
ELI  SORROW,  MD 
CLAY  A.  WAGGENSPACK,  JR,  MD 
WINSTON  H.  WEESE,  MD 
PATRICK  W.  PEAVY,  MD 


Established  1844.  Owned  and  edited  by  The 
; Journal  of  the  Louisiana  State  Medical  Society,  Inc., 
1700  Josephine  Street,  New  Orleans,  LA  70113. 

Copyright  1988  by  The  Journal  of  the  Louisiana 
State  Medical  Society,  Inc. 

Subscription  price  is  $12  per  year  in  advance, 
postage  paid  for  the  United  States;  $15  per 
year  for  all  foreign  countries  belonging  to  the 
Postal  Union;  $1.50  per  single  issue. 

Advertising:  Contact  Sissy  Sullivan  Hansen, 
1700  Josephine  Street,  New  Orleans,  LA  70113; 

(504)  561-1033,  (800)  462-9508. 

Postmaster:  Send  address  changes  to  1700 
Josephine  Street,  New  Orleans,  LA  70113. 

The  JOURNAL  (ISSN  0024-6921)  is  published 
monthly  at  1700  Josephine  Street,  New 
Orleans,  LA  70113.  Second-class  postage  paid 
at  New  Orleans  and  additional  mailing  offices. 

Articles  and  advertisements  published  in  the 
JOURNAL  are  for  the  interests  of  its  readers  and 
do  not  represent  the  official  position  or 
endorsement  of  The  Journal  of  the  Louisiana  State 
Medical  Society,  Inc.  or  the  Louisiana  State 
Medical  Society.  The  JOURNAL  resers'es  the 
right  to  make  the  final  decision  on  all  content 
and  advertisements. 


JOURNAL 

OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY  1988 

VOLUME  140  / NUMBER  1 / JANUARY 


ARTICLES 


3 

Official  Call  for  the  1988 
House  of  Delegates 

Terry  R.  Jones,  MD 
John  D.  Fmsha,  MD 
Jon  V.  Schellack,  MD 

28 

Traumatic  occupational 
occlusive  arterial  disease 
of  the  hands 

David  J.  Holcombe,  MD 

37 

A case  of  metastatic 
carcinoma  in  association 
with  Paget's  disease 
of  bone 

Irwin  Cohen,  MD 

41 

A community  medicine 
program  in  Jamaica  for 
fourth  year  medical 
students 

DEPARTMENTS 

2 

Information  for  Authors 

5 

New  Members 

9 

ECG  of  the  Month 

13 

Otolaryngology/Head  & 

Neck  Surgery  Report 

22 

Calendar 

24 

Auxiliary  Report 

51 

Classified  Advertising 

52 

Books  Received 

Cover  illustration  by  Eugene  New,  New  Orleans. 


INFORMATION  FOR  AUTHORS 


The  JOURNAL  of  the  Louisiana  State  Medical  Society  is  intended  to 
provide  practical  scientific  information  of  interest  to  a broad  spectrum 
of  physician  members  of  the  LSMS  and  to  meet  the  need  of  each  physi- 
cian to  maintain  a general  awareness  of  progress  and  change  in  clinical 
medicine.  The  content  is  designed  to  aid  the  practicing  physician  in 
giving  comprehensive  care  and  in  recognizing  the  need  for  special- 
ized treatment. 

The  JOURNAL  welcomes  material  for  publication  if  submitted  in  ac- 
cordance with  the  following  guidelines.  Address  all  correspondence 
to  the  Editor,  Journal  of  the  Louisiana  State  Medical  Society,  1700 
Josephine  Street,  New  Orleans,  LA  701 1 3.  Contact  the  managing  editor 
with  any  questions  concerning  these  guidelines  or  for  a checklist  to 
assist  in  manuscript  preparation. 

MANUSCRIPTS  should  be  of  an  appropriate  length  due  to  the  policy 
of  the  JOURNAL  to  feature  concise  but  complete  articles.  (Some  sub- 
jects may  necessitate  exception  to  this  policy  and  will  be  reviewed 
and  published  at  the  Editor's  discretion.)  The  language  and  vocabulary 
of  the  manuscript  should  be  understandable  and  not  beyond  the  com- 
prehension of  the  general  readership  of  the  journal.  The  journal 
attempts  to  avoid  the  use  of  medical  jargon  and  abbreviations.  All  ab- 
breviations, especially  of  laboratory  and  diagnostic  procedures,  must 
be  identified  in  the  text.  Manuscripts  must  be  typed,  double-spaced 
with  adequate  margins.  (This  applies  to  all  manuscript  elements  in- 
cluding text,  references,  legends,  footnotes,  etc.)  The  original  and  one 
duplicate  should  be  submitted.  An  accompanying  cover  letter  should 
designate  one  author  as  correspondent  and  include  his/her  address 
and  telephone  number.  Manuscripts  are  received  with  the  explicit 
understanding  that  they  have  not  been  previously  published  and  are 
not  under  consideration  by  any  other  publication.  Manuscripts  are  sub- 
ject to  editorial  revisions  as  deemed  necessary  by  the  editors  and  to 
such  modifications  as  to  bring  them  into  conformity  with  journal 
style.  Statements  made  or  opinions  expressed  by  any  contributor  in 
any  article  or  feature  published  in  the  journal  are  the  sole  respon- 
sibility of  the  author. 

REVIEWING  PROCESS.  Each  manuscript  is  reviewed  by  the  Editor 
and  by  a member(s)  of  the  Editorial  Board  or  the  Panel  of  Consultants 
from  whom  knowledgeable  opinions  are  sought.  The  acceptability  of 
a manuscript  is  determined  by  such  factors  as  the  quality  of  the 
manuscript,  perceived  interest  to  journal  readers,  usefulness  or  im- 
portance to  physicians,  and  the  current  backlog  of  accepted 
manuscripts.  Authors  are  notified  upon  receipt  of  the  manuscript.  When 
acceptability  is  determined,  authors  will  then  be  requested  to  sign  a 
manuscript  consent  form  transferring  copyright  privileges  to  the  jour- 
nal. Accepted  manuscripts  become  the  property  of  the  journal  and 
may  not  be  published  elsewhere,  in  part  or  in  whole,  without  permis- 
sion from  the  journal.  Abstracts  may  be  reproduced  without  specific 
permission,  provided  acknowledgement  of  the  source  is  made. 

TITLE  PAGE  should  carry  [1]  the  title  of  the  manuscript,  which  should 
be  concise  but  informative;  [2]  full  name  of  each  author,  with  highest 
academic  degree(s),  listed  in  descending  order  of  magnitude  of  con- 
tribution (only  the  names  of  those  who  have  contributed  materially 
to  the  preparation  of  the  manuscript  should  be  included);  [3]  a one- 
to  two-sentence  biographical  description  for  each  author  which  should 
include  specialty,  practice  location,  academic  appointments,  primary 
hospital  affiliation,  or  other  credits  (a  picture,  black-and-white  head 
shot,  of  each  author  may  also  be  sent  if  available);  [4]  name  and  ad- 
dress of  author  to  whom  requests  for  reprints  should  be  addressed, 
or  a statement  that  reprints  will  not  be  available. 

ABSTRACT  should  be  on  the  second  page  and  consist  of  no  more  than 
150  words.  It  is  designed  to  acquaint  the  potential  reader  with  the 
essence  of  the  text  and  should  be  informative  rather  than  descriptive. 
(Avoid  telling  what  "will  be  described"  and  instead  describe  it.)  The 
abstract  should  be  intelligible  when  divorced  from  the  article,  devoid 
of  undefined  abbreviations,  and  suitable,  without  rewriting,  for 
reproduction  by  abstracting  services.  The  abstract  should  contain:  [1] 
a brief  statement  of  the  manuscript's  purpose;  [2]  the  approach  used; 
[3]  the  material  studied;  [4]  the  results  obtained.  Emphasize  new  and 
important  aspects  of  the  study  or  observations. 


KEY  WORDS  should  follow  the  abstract  and  be  identified  as  such. 
Provide  three  to  five  key  words  or  short  phrases  that  will  assist  index- 
ers in  cross-indexing  your  article.  Use  terms  from  the  Medical  Sub- 
ject Heading  list  from  Index  Medicus  when  possible. 

SUBHEADS  are  strongly  encouraged.  They  should  provide  guidance 
for  the  reader  and  serve  to  break  the  typographic  monotony  of  the 
text.  The  format  is  flexible  but  subheads  ordinarily  include:  Methods 
and  Materials,  Case  Reports,  Symptoms,  Examination,  Treatment  and 
Technique,  Results,  Discussion,  and  Summary. 

REFERENCES  must  be  double-spaced  on  a separate  sheet  of  paper  and 
limited  to  a reasonable  number.  They  will  be  critically  examined  at 
the  time  of  review  and  must  be  kept  to  a minimum.  All  references 
must  be  cited  in  the  text  and  the  list  should  be  arranged  in  order  of 
citation,  not  alphabetically.  Personal  communications  and  unpublished 
data  should  not  be  included  in  references,  but  should  be  incorporated 
in  the  text.  The  following  form  should  be  followed: 

JOURNALS 

[1]  Author(s):  Use  the  surname  followed  by  initials  without  punctua- 
tion. The  names  of  all  authors  should  be  given  unless  there  are  more 
than  three,  in  which  case  the  names  of  the  first  three  authors  are 
used,  followed  by  "et  al."  [2]  Title  of  article.  Capitalize  only  the  first 
letter  of  the  first  word.  [3]  Name  of  journal  Followed  by  no  punrtua- 
tion,  underscored,  and  abbreviated  according  to  Index  Medicus.  [4] 
Year  of  publication;  [5]  Volume  number:  Do  not  include  issue  number 
or  month  except  in  the  case  of  a supplement  or  when  pagination  is 
not  consecutive  throughout  the  volume.  [6]  Inclusive  page  numbers. 
Do  not  omit  digits. 

Example:  Bora  LI,  Dannem  FJ,  Stanford  W,  et  al:  A guideline  for  blood 

use  during  surgery.  Am  j Clin  Pathol  1 979;71 :680-692. 

BOOKS 

[1]  Author(s):  Use  the  surname  followed  by  initials  without  punctua- 
tion. The  names  of  all  authors  should  be  given  unless  there  are  more 
than  three,  in  which  case  the  names  of  the  first  three  authors  are  used 
followed  by  "et  al."  [2]  Title,  Capitalize  the  first  and  last  word  and 
each  word  that  is  not  an  article,  preposition,  or  conjunction  of  less 
than  four  letters.  [3]  Edition  number,  [4]  Editor's  name.  [5J  Place  of 
publication,  [6]  Publisher,  [7]  Year,  [8]  Inclusive  page  numbers.  Do 
not  omit  digits. 

Example:  DeCole  EL,  Spann  E,  Flurst  RA  Jr,  et  al:  Bedside  Examina- 

tion in  Cardiovascular  Medicine,  ed  2,  Smith  JT  (ed).  New 
York,  McGraw  Hill  Co,  1986,  23-37. 

ILLUSTRATIONS  should  be  submitted  in  duplicate  in  an  envelope 
(paper  clips  should  not  be  used  on  illustrations  since  the  indentation 
they  make  may  show  on  reproduction).  Legends  should  be  typed  on 
a separate  sheet  of  paper.  Photographic  material  should  be  high-contrast 
glossy  prints.  Patients  must  be  unrecognizable  in  photographs  unless 
specific  written  consent  has  been  obtained,  in  which  case  a copy  of 
the  authorization  should  accompany  the  manuscript.  Omit  illustra- 
tions which  do  not  increase  understanding  of  text.  Illustrations  must 
be  limited  to  a reasonable  number  (four  illustrations  should  be  ade- 
quate for  a manuscript  of  4 to  5 typed  pages).  The  following  informa- 
tion should  be  typed  on  a label  and  affixed  to  the  back  of  each  il- 
lustration: figure  number,  title  of  manuscript,  name  of  senior  author, 
and  arrow  indicating  top. 

TABLES  should  be  self-explanatory  and  should  supplement,  not 
duplicate,  the  text.  Each  should  be  typed  on  a separate  sheet  of  paper, 
numbered,  and  have  a brief  descriptive  title. 

ACKNOWLEDGMENTS  are  the  author's  prerogative;  however, 
acknowledgment  of  technicians  and  other  remunerated  personnel  for 
carrying  out  routine  operations,  or  of  resident  physicians  who  merely 
care  for  patients  as  part  of  their  hospital  duties  is  discouraged.  More 
acceptable  acknowledgments  include  those  of  intellectual  or  profes- 
sional participation. 

GALLEY  PROOFS  will  be  mailed  to  the  principal  author  for  correc- 
tions. Reprint  orders  forms  will  accompany  galley  proofs. 


OFFICIAL 

CALL 


FOR  THE  1988  HOUSE  OF  DELEGATES  □ MARCH  11-13,  1988 


IN  ACCORDANCE  WITH  the  constitution  and  bylaws  of  the  Louisiana  State  Medical  Society,  the  House  of  Delegates  is  being 
called  into  annual  session  at  9 am,  Friday,  March  11,  1988  at  the  Le  Centre  Civique  in  Lake  Charles,  Louisiana.  The  House  will 
consider  such  business  as  presented  and  required  of  its  annual  session.  The  House  will  be  called  to  order  in  the  usual  manner 
and  remain  in  session  until  its  duties  are  complete. 


The  delegation  representation  of  the  component  societies  in  the  House  for  the  1988  Annual  Meeting  is  as  follows: 


Acadia 

2 

East  Baton  Rouge 

28 

Natchitoches 

1 

St  Mary 

2 

Allen 

1 

East  & West  Feliciana  1 

North  Central 

3 

St  Tammany 

7 

Ascension 

1 

Evangeline 

2 

Orleans 

59 

Shreveport 

24 

Assumption 

1 

Franklin 

1 

Ouachita 

12 

Tangipahoa 

4 

Avoyelles 

1 

Iberia 

3 

Pointe  Coupee 

1 

Terrebonne 

5 

Beauregard 

1 

Iberville 

1 

Rapides 

9 

Tri-Parish 

1 

Bossier 

2 

Jefferson 

22 

River  Parishes 

2 

Vermillion 

2 

Calcasieu 

10 

Jefferson  Davis 

1 

Sabine 

1 

Vernon 

1 

Catahoula-Concordia 

1 

Lafayette 

13 

St  Bernard 

2 

Washington 

2 

Claiborne 

1 

Lafourche 

4 

St  Landry 

3 

Webster 

1 

DeSoto 

1 

Morehouse 

1 

St  Martin 

1 

The  current  general  officers,  delegates  to  the  AMA,  past  presidents,  past  speakers  of  the  House,  journal  editor,  emeritus  of- 
ficers, district  societies  and  one  representative  from  each  medical  school  are  also  members  of  the  House  of  Delegates.  The  Medical 
Student  Section  is  entitled  to  three  delegates  and  three  alternate  delegates.  The  Resident  Physician  Section  is  entitled  to  one  delegate 
and  one  alternate. 


Component  societies 

242 

District  societies 

10 

Medical  schools 

3 

Delegates  and  alternate  delegates  to  the  AMA 

10 

Medical  Student  Section 

3 

General  officers,  past  presidents,  past  speakers  of  the  House, 

Resident  Physician  Section 

1 

JOURNAL  editor  and  emeritus  officers 

32 

Total  Delegates 

301 

REGISTRATION  facilities  will  be  maintained  for  delegates,  alternate  delegates,  officers,  executives  of  the  component  medical 
societies  and  invited  guests.  Registration  hours  will  be  as  follows: 

Lake  Charles  Hilton  Le  Centre  Civique 

Thursday,  March  10  1 - 5 pm  Friday,  March  11  8 am  - 5 pm 

Saturday,  March  12  8 am  - 5 pm 

Sunday,  March  13  8 am  - noon 


JOURNAL  VOL  140  JANUARY  3 


To  help  him  rebuild  his  life,  you  have 
many  alternatives  but  only  one  choice 
for  comprehensive  rehab  services. 


Many  hospitals  offer  rehab 
services,  but  only  the  Rehabilitation 
Institute  of  New  Orleans  can  offer 
your  patient  the  comprehensive 
range  of  services  he  needs  to  fully 
explore  his  capabilities  and  realize 
his  potential. 

As  the  largest  full-service  acute 
care  rehabilitation  hospital  in  the 
Gulf  Coast  region,  F.  Edward  Hebert 
is  the  primary  referral  center  for 
Louisiana  and  neighboring  states. 

Our  diagnosis-related  treatment 
teams  are  separate  and  complete  for 
each  disability  category:  spinal  cord 
injury,  brain  trauma,  stroke,  limb 
loss,  bums,  arthritis,  neuromuscular 
disorders,  multiple  trauma,  and 
related  disorders.  These  teams  of 
specialists  provide  tightly  focused 
inpatient  and  outpatient  care  to 


achieve  the  best  possible  results  in 
the  briefest  possible  time. 

At  the  Rehabilitation  Institute 
of  New  Orleans,  we  rebuild  lives. 


Rehabilitation  Institute 
Of  New  Orleans 

We  ReBuild  lives 

F.  EDWARD  HEBERT  HOSPITAL 
One  Sanctuary  Drive,  New  Orieans,  LA  70114,  (504)  363-22(X) 
METAIRIE  OUTPATIENT  SERVICES 
3001  Division  Street  ^^200,  Metairie,  LA  70002,  (504)  454-7276 

^1  Subsidiaries  of  Rehab  Hospital  Services  Corporation 


4 JOURNAL  VOL  140  JANUARY 


NEW  MEMBERS 


Applications  for  membership  have  been  re- 
ceived from  the  following  physicians  by  the 
respective  parish  medical  societies  as  of  Oc- 
tober 7,  1987.  The  Louisiana  State  Medical 
Society  is  pleased  to  welcome: 

■ Lafayette 

Richard  L.  Fremaux,  MD 

PO  Box  39700,  Lafayette  70503 

1969,  LSU  School  of  Medicine,  New  Orleans 

diagnostic  radiology 

Arlene  C.  Richard,  M.D, 

606  Haifleigh,  Franklin  70538 

1983,  Howard  University  College  of  Medi- 
cine, Washington,  DC 

family  practice 

■ Orleans 

Malcolm  E.  Andry  Jr,  MD 

3439  Prytania,  New  Orleans  70115 
1982,  Tulane  University  School  of  Medicine 
internal  medicine 

Charles  K.  Angelo  Jr,  MD 

1202  Monroe  St,  Gretna  70053 
1985,  LSU  School  of  Medicine,  New  Orleans 
-general  practice 

Joanell  M.  Darnell,  MD 

1328  Ahne  St,  New  Orleans  70115 
1980,  LSU  School  of  Medicine,  New  Orleans 
obstetrics/ gynecology 

George  D.  MacEwen,  MD 

200  Henry  Clay  Ave,  New  Orleans  70118 
1953,  Queens  University  Faculty  of  Medi- 
cine, Ontario,  Canada 
orthopedic  surgery 

William  S.  Riggins  Jr,  MD 

4700  General  Meyer  #208,  New  Orleans 
70130 

1984,  LSU  School  of  Medicine,  Shreveport 
family  practice 

Jean  Ann  Tolmas,  MD 

2017  Metairie  Rd,  Metairie  70005 

1980  Tulane  University  School  of  Medicine 

pediatrics 


■ Ouachita 

Brian  W.  Alexander,  MD 

2001  Royal  Ave,  Monroe  71201 
1984,  University  of  Arkansas  School  of 
Medicine 
anesthesiology 

J,  Michael  Barraza,  MD 

3315  Deborah  Dr,  Monroe  71201 

1982,  Tulane  University  School  of  Medicine 

diagnostic  radiology 

Francis  Capalongan,  MD 

1006  Winnsboro  Rd,  Monroe  71202 
1975,  Faculty  of  Medicine  and  Surgery  Uni- 
versity of  Santo  Tomas,  Manila,  Philip- 
pines 
pathology 

Dan  B.  Davidson,  MD 

3421  Medical  Park  Dr,  Monroe  71211 
1975,  University  of  Mississippi  School  of 
Medicine 
diagnostic  radiology 

Noli  C.  Guinigundo,  MD 

1300  North  Seventh  St,  West  Monroe  71291 
1962,  Institute  of  Medicine  Far  Eastern  Uni- 
versity, Manila,  Philippines 
family  practice 

Robert  D.  Halsell,  MD 

2204  Justice  St,  Monroe  71201 

1982,  LSU  School  of  Medicine,  Shreveport 

radiology 

William  J.  Liles  Jr,  MD 

PO  Box  8357,  Monroe  71211 

1979,  LSU  School  of  Medicine,  Shreveport 

pathology 

Scott  K.  McClelland,  MD 

3510  Medical  Park  Dr,  Monroe  71203 
1982,  LSU  School  of  Medicine,  Shreveport 
orthopedic  surgery 

Owen  M.  Meyers,  MD 
714  St  John,  Monroe  71201 
1984,  University  of  Mississippi  School  of 
Medicine 
family  practice 


James  T.  Rittelmeyer,  MD 

3510  Medical  Park  Dr,  Monroe  71203 
1978,  Georgetown  University  School  of 
Medicine 
cardiology 

Joaquin  P.  Rosales,  MD 

104  Contempo,  West  Monroe  71291 

1984,  LSU  School  of  Medicine,  New  Orleans 

pediatrics 

Michael  J.  Sampognaro,  MD 

2810  Armand,  Monroe  71201 

1984,  LSU  School  of  Medicine,  New  Orleans 

internal  medicine 

Richard  V.  Vines  II,  MD 

312  Grammont  #301,  Monroe  71201 

1984,  LSU  School  of  Medicine,  Shreveport 
internal  medicine 

■ Intern/ Resident  Members 

ORLEANS 

Stanley  M.  Bienasz,  MD 

808  Tullulah,  River  Ridge  70123 

1985,  Tulane  University  School  of  Medicine 
anesthesiology 

Adrian  B.  Blotner,  MD 

1516  Jefferson  Hwy,  New  Orleans  70121 
1984,  LSU  School  of  Medicine,  New  Orleans 
psychiatry 

Luis  G.  Uribe,  MD 

1213  Colony  Rd,  Metairie  70003 
1980,  Facultad  de  Medicina  de  la  Univer- 
sidad  del  Valle,  Colombia 
internal  medicine 


ERRATUM 

On  page  3 of  the  November  1987  issue 
of  the  JOURNAL,  it  was  stated  that 
Gail  C.  Brady,  MD  was  a new 
member  specializing  in  internal 
medicine.  Dr.  Brady  practices 
psychiatry  in  Jefferson  Parish.  The 
JOURNAL  regrets  the  error. 


JOURNAL  VOL  140  JANUARY  5 


Crisis  in  black  and  white. 


Your  personal  crisis  may  be  waiting  in  the 
morning  mail.  If  so,  you’ll  want  the  best 
professional  help.  You’ll  want  a Medical 
Protective  General  Agent. 

Professional  liability  coverage  is  our  only 
business.  And  we’ve  been  providing  it  for 
almost  100  years.  Our  agents  live  in  the 
territories  they  serve  so  they  understand  the 
local  legal  climate.  And  with  the  extensive 


resources  of  the  home  office  Law  Depart- 
ment to  draw  from,  they’re  always  ready  to 
answer  your  questions  or  give  advice. 

Someday  it  may  be  you  against  a negligence 
charge.  When  that  day  comes  and  your 
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going  to  want  all  the  help  you  can  get.  To 
make  sure  you  have  it,  contact  your  Medical 
Protective  General  Agent  today. 


1 at,)  t/.MOf a 

Dale  Weaver 

2900  West  Fork  Drive,  Suite  200,  Baton  Rouge,  LA  70827,  (504)  291-1807 


Norton  W.  Voorhies,  MD,  Editor 


ECG  OF  THE  MONTH 


TOO  LONG  TO  WAIT 


JORGE  I.  MARTINEZ-LOPEZ,  MD 


The  rhythm  strip  shown  below,  precordial  lead  VI,  was  recorded  in  a 74-year-old  woman  shortly  after 
her  admission  to  the  hospital  with  a clinical  diagnosis  of  acute  pancreatitis. 


What  is  your  diagnosis?  Elucidation  is  on  page  11. 


JOURNAL  VOL  140  JANUARY  9 


PHYSICIANS, 
SCHEDULE 
SOME  TIME  FOR 
YOUR  COUNTRY. 

Many  physicians  would 
like  to  devote  some  time  to  their 
country  in  a local  Army  Reserve 
unit.  We  know  that  making  a 
weekend  commitment  can  be 
difficult  for  most  physicians.  So  it 
is  practical  for  the  Army  Reserve 
units  to  be  flexible  about  time. 
It’s  worth  discussing. 

Incidentally,  in  addition 
to  satisfying  your  own  desire  to 
serve  your  country,  there  are 
exceptional  opportunities  to  do 
something  totally  different  from 
a day-to-day  routine.  Oppor- 
tunities to  study  new  areas  of 
medicine,  meet  new  people  in 
your  specialty,  and  be  a part  of 
one  of  the  world  ’s  most  advanced 
medical  teams. 

Discuss  the  opportunities 
with  our  Army  Medical  Person- 
nel Counselor. 


FOR 

SURGEONS 
LOOKING  FOR 
ACHAUENGE. 

Your  challenge  could  be  the 
Army  Reserve  unit  near  you.  It’s  a 
unit  that  requires  the  services  of 
surgeons. 

You  may  wish  to  explore  the 
challenge  of  teaching  in  a major 
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grams in  which  you’ll  be  able  to 
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country. 

The  Army  Reserve  understands 
the  time  demands  on  a busy  physi- 
cian, so  you  can  count  on  us  to  be 
totally  flexible  in  making  time  for  you 
to  share  your  specialty  with  your 
country.  We’ll  arrange  your  training 
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To  find  out  about  the  benefits  of 
serving  with  a nearby  Army  Reserve 
unit,  we  recommend  you  call  our 
Armv  Medical  Personnel  Counselor. 


PHYSICIANSJHERE 
ARE  TWO  KINDS 
OF  FLEXIBILITY  IN 
THE  ARMY  RESERVE 
WE  THINK  YOU'LL  LIKE. 

One,  time.  We  know  how 
tough  it  is  for  a busy  physician 
to  make  weekend  time  commit- 
ments. So  we  offer  flexible 
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physician  to  share  some  time 
with  his  or  her  country.  We 
arrange  a schedule  to  suit  your 
requirements. 

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explore  other  phases  of  medi- 
cine, to  add  a different  kind  of 
knowledge— the  challenge  of 
military  health  care.  It’s  a flexi- 
bility which  could  prove  to  be 
both  stimulating  and  reward- 
ing, with  the  opportunity  to 
participate  in  a variety  of 
programs  that  can  put  you  in 
contact  with  medical  leaders 
from  all  over  the  country. 

See  how  flexible  we  can 
be,  call  our  Army  Medical 
Personnel  Counselor. 


ARMY  RESERVE. 
BEAUYOUCANBE. 


HERE'S  ONE  DOCTOR 
WHO  WON'T  PAY 
HIS  MALPRACTICE 
PREMIUMS  THIS  YEAR. 

The  Army  covers  his  premiums. 
Since  he’s  an  Army  Physician,  there  are 
a lot  ofworries  associated  with  private 
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with.  Like  excessive  paperwork,  and  the 
overhead  costs  incurred  in  running  a 
private  practice. 

What  he  will  get  is  a highly  challeng- 
ing, highly  rewardingexperience.  The 
Armyoffers  varied  assignments, 
chances  tospecialize,  orfurtheryour 
education,  and  to  work  with  a team  of 
dedicated  health  care  professionals. 

Plus  a generous  benefits  package. 

Ifyou'rc  interested  in  practicinghigh 
quality  health  care  with  a minimum  of 
administrative  burdens,  examine  Army 
medicine.  T alk  toyourlocal  Army 
Medical  Department  Counselor  for 
more  information. 

ARMY  MEDICINE. 
BEAUYOUCANBE. 


MAJOR  OPPORTUNITIES  FOR 
HEALTH  PROFESSIONALS. 


Army/Army  Reserve  Medicine 
144  Elk  Place,  Suite  1514 
New  Orleans,  LA  701 12 
Call  collect:  (504)  589-2373 


ECG  of  the  Month 

Case  presentation  is  on  page  9. 

DIAGNOSIS  — Second-degree  AV  block  and  ventricular 
escape  rhythm 

The  basic  cardiac  rhythm  is  sinus  at  72  times  a minute. 

Prominent  in  the  rhythm  strip  are  three  impor- 
tant features.  First,  some  sinus  P waves  are  con- 
ducted, while  others  are  not.  Second,  two  different 
types  of  QRS  complexes  are  present.  Third,  the  tem- 
poral relationship  of  the  P waves  to  the  QRS  com- 
plexes is  not  constant.  The  significance  of  these  three 
findings  will  be  explored  further  in  the  discussion  to 
follow. 

To  facilitate  the  interpretation  of  the  tracing  and 
the  discussion  that  follows,  use  the  fifth  P wave  on 
the  top  panel  as  the  point  of  departure. 

DISCUSSION 

Sinus  rhythm  is  signaled  in  the  tracing  by  the  regular 
appearance  of  P waves  at  rates  of  72  times  a minute. 
Ventricular  electrical  activity,  on  the  other  hand,  is 
characterized  by  the  presence  of  QRS  complexes  with 
two  very  different  morphologies:  one  is  narrow,  neg- 
atively oriented,  and  is  followed  by  a normal  T wave; 
the  other  is  abnormally  wide  (0.12  sec),  has  an  rsR' 
pattern,  and  is  followed  by  secondary  ST-T  wave  ab- 
normalities. 

The  P-R  interval  between  the  fifth  P wave  and 
the  narrow  QRS  that  follows  it  is  normal  (0.18  sec). 
The  next  PR  interval,  however,  lengthens  to  0.26  sec. 
Measurement  of  subsequent  PR  intervals  reveals  that 
the  interval  associated  with  the  seventh  P remains  at 
0.26  sec,  while  that  of  the  eighth  P lengthens  to  0.28 
sec,  and  remains  unchanged  with  the  ninth  and  tenth 
P waves.  In  the  second  panel  of  the  rhythm  strip,  the 
PR  interval  associated  with  the  first  P increases  further 
to  0.32  sec,  and  the  next  P is  not  conducted.  Similar 
sequences  are  recorded  throughout  the  tracing  wher- 
ever narrow  QRS  complexes  are  inscribed.  In  other 
words,  sinus  P waves  keep  temporal  relationship  with 
the  narrow  QRS  complexes,  but  PR  intervals  pro- 
gressively lengthen  until  a P wave  is  not  conducted. 
This  pattern  is  consistent  with  the  ECG  diagnosis  of 
second-degree,  Mobitz  1 AV  block  (or  Wenckebach  pe- 
riodicity). Because  the  PR  intervals  lengthen,  then 


remain  static  before  lengthening  again,  the  pattern 
represents  a so-called  atypical  form  of  Mobitz  I AV 
block.  The  three  sequences  recorded  in  the  tracing 
represent  AV  ratios  of  8:7, 11:10,  and  9:8  respectively. 

Second-degree,  Mobitz  I AV  block  is  the  result 
of  a conduction  disorder  at  the  AV  junctional  level. 
During  sinus  rhythm,  and  in  the  absence  of  concom- 
itant bundle  branch  block,  ventricular  complexes  are 
narrow,  denoting  normal  distal  intraventricular  con- 
duction. 

Pauses  occasioned  by  non-conducted  sinus  P 
waves  may  be  interrupted  or  terminated  in  several 
ways:  by  the  appearance  of  a subsequent  sinus  P wave, 
ectopic  premature  impulses,  ectopic  escape  impulses, 
or  ectopic  escape  rhythms.  The  second  panel  of  the 
rhythm  strip  shows  four  consecutive  wide  QRS  com- 
plexes after  the  non-conducted  sinus  P.  The  first  of 
the  four  QRS  complexes  occurs  after  a long  pause 
(0.96  sec  after  the  preceding  narrow  QRS).  Therefore, 
this  wide  QRS  is  not  a premature  ventricular  impulse, 
but  a ventricular  escape  impulse.  Moreover,  the  brief 
sequence  of  four  consecutive  wide  QRS  complexes 
represents  a ventricular  escape  rhythm  at  rates  of  65 
times  a minute.  Other  similar  sequences  are  found 
throughout  the  tracing.  Of  interest  is  the  fact  that  the 
escape  interval  is  not  constant;  it  is  either  equal  to  or 
longer  than  the  R-R  interval  during  the  escape  rhythm 
(0.76  sec). 

The  location  of  the  Ps,  with  respect  to  the  wide 
QRS  complexes,  has  no  effect  on  either  the  escape 
interval  or  the  firing  rate  of  the  ectopic  ventricular 
site.  This  finding  provides  another  ECG  diagnosis: 
there  is  A-V  dissociation  during  the  sequences  of  ven- 
tricular escape  rhythm. 

Now,  back  to  the  wide  QRS  complexes.  Already 
established  is  the  fact  that  they  are  caused  by  a ven- 
tricular escape  mechanism  at  rates  of  65  times  a min- 
ute. On  this  basis,  two  ventricular  rhythms  can  be 
excluded:  the  ventricular  rate  is  too  slow  for  ventric- 
ular tachycardia  and  too  fast  for  idioventricular 
rhythm.  The  escape  rhythm  is  due  to  accelerated  idio- 
ventricular rhythm  (AIVR). 

Criteria  for  the  ECG  diagnosis  of  AIVR  include 
the  following:  1)  ectopic  ventricular  rhythm  with  rates 
of  50  to  125  times  a minute,  2)  initiation  of  the  rhythm 
by  an  escape  impulse  or  a fusion  beat  appearing  dur- 
ing slowing  of  the  sinus  rate  or  during  partial  AV 
block,  3)  a regular  R-R  interval,  and  4)  termination 
with  a return  to  the  basic  rhythm,  with  or  without  ^ 

JOURNAL  VOL  140  JANUARY  11 


YOCON' 

YOHIMBINE  HCI 


Oescriptfim:  Yohimbine  is  a 3a-15a-20B-17a-hydroxy  Yohimblne-ISa-car- 
boxylic  acid  methyl  ester.  The  alkaloid  is  found  in  Rubaceae  and  relatedtrees. 
Also  in  Rauwolfia  Serpentina  (1)  Benth.  Yohimbine  is  an  indolalkylamine 
alkaloid  with  chemical  similar!^  to  reserpine.  It  is  a crystalline  powder, 
odorless.  Each  compressed  tablet  contains  (1/12  gr.)  5.4  mg  of  Yohimbine 
Hydrochloride. 

Actiwi:  Yohimbine  blocks  presynaptic  atpha-2  adrenergic  receptors.  Its 
action  on  peripheral  blood  vessels  resembles  that  of  reserpine,  though  it  is 
» weaker  arid  of  short  duration.  Yohimbine’s  peripheral  autonomic  nervous 
system  effect  Is  to  increase  parasympathetic  (cholinergic)  and  decrease 
sympattietlc  (adrenergic)  activity.  It  is  to  be  noted  that  in  male  sexual 
performance,  erection  is  linked  to  cholinergic  activity  and  to  alpha-2  ad- 
renergic blockade  which  may  ttteoretically  result  in  increased  penile  inflow, 
decreased  penile  outflow  or  both. 

Yohimbine  exerts  a stimulating  action  on  the  mood  and  may  increase 
anxiety.  Such  actions  have  not  been  adequately  studied  or  related  to  dosage 
although  they  appear  to  require  high  doses  of  the  drug . Yohimbine  has  a mild 
anti-diuretic  action,  probably  via  stimulation  of  hypothalmic  centers  and 
release  of  posterior  pituitary  hormone. 

Reportedly,  Yohimbine  exerts  no  significant  influence  on  card'rac  stimula- 
tion and  other  effects  mediated  by  B-adrenergic  receptors,  its  effect  on  blood 
pressure,  if  any,  would  be  to  lower  it;  however  no  adequate  studies  are  at  hand 
to  quafrttate  this  effect  irt terms  of  Yohimbine  dosage. 

Indications:  Yocon®  is  indicated  as  a sympathicolytlc  and  mydriatric.  It  may 
have  activity  as  an  aphrodisiac. 

Contraindintions:  Renal  diseases,  and  patient’s  sensitive  to  Ihe  drug.  In 
view  of  die  limited  and  inadequate  information  at  hand,  no  precise  tabulation 
can  be  offered  of  additional  contraindications. 

VVarnlim:  Generally,  this  drug  is  not  proposed  for  use  in  females  and  certainly 
must  not  be  used  during  pregnancy.  Neither  is  this  drug  proposed  for  use  in 
pediatric,  geriatric  or  cardio-renal  patients  with  gastric  or  duodenal  ulcer 
history.  Nor  should  it  be  used  in  conjunction  with  mood-modifying  drugs 
such  as  antidepressants,  or  in  psychiatric  patients  in  general. 

Adverse  Reactions:  Yohimbine  readily  penetrates  the  (CNS)  and  produces  a 
complex  pattern  of  responses  in  lower  doses  than  required  to  produce  periph- 
eral  a-adrenergic  blockade.  These  include,  anti-diuresis,  a general  picture  of 
* central  excitation  including  elevation  of  blood  pressure  and  heart  rate,  in- 
creased motor  activity,  irritability  and  tremor.  Sweating,  nausea  and  vomiting 
are  common  after  parenteral  administration  of  the  drug.^  ^ Also  dininess, 
headache,  skin  flushing  repotted  when  used  orally,  f 3 
Dosage  and  Administration:  Experimental  dosage  reported  in  treatment  of 
erectile  impotence.  T3,4  -|  tablet  (5.4  mg)  3 times  a day,  to  adult  males  taken 
orally.  Occasional  side  effects  reported  with  this  dosage  are  nausea,  dizziness 
or  nervousness.  In  the  event  of  side  effects  dosage  to  be  reduced  to  Vi  tablet  3 
times  a day.  followed  by  gradual  increases  to  1 tablet  3 times  a day.  Reported 
therapy  not  more  than  10  weeks. 3 
How  Applied:  Oral  tablets  of  Yocon®  1/12  gr.  5.4  mg  in 
bottles  of  100’s  NDC  53159-001-01  and  1000’s  ^ 

53159-001*10.  4"  ^^***'^ 

References; 

1.  A-  Morales  et  al..  New  England  Journal  of  Medi- 
cine: 1 221 . November  12 . 1981 . 

2.  Goodman,  Gilman  — The  Pharmacological  basis 
of  Therapeutics  6th  ed , , p . 1 76  - 1 88. 

McMillan  December  Rev.  1/85. 

3.  Weekly  Urological  Clinical  letter,  27:2,  July  4, 

1983. 

4.  A.  Morales  et  al. , The  Journal  of  Urology  128: 

45-47, 1982. 

Rev.  1/85 


AVAILABLE  EXCLUSIVELY  FROM 

PALISADES 

PHARMACEUTICALS,  INC. 

219  County  Road 
Tenafly,  New  Jersey  07670 

(201)  569-8502 
Outside  NJ  1-800-237-9083 


fusion  beats.  The  morphology  of  the  wide  QRS  com- 
plexes during  AIVR  is  uniform  in  most  instances.  On 
rare  occasions,  multiform  AIVR  (ie,  displaying  at  least 
two  different  QR  morphologies)  can  occur. 

The  combination  of  second-degree,  Mobitz  I 
A-V  block  with  AIVR  is  not  a common  one.  In  this 
patient,  AIVR  surfaces  when  a subsidiary  pacemaker 
in  the  ventricular  musculature  decides  that  the  pause 
created  by  the  A-V  block  is  “too  long  to  wait  for." 
Therefore,  the  subsidiary  pacemaker  fires,  at  times 
resulting  in  a single  escape  impulse  or  in  a non-sus- 
tained  burst  of  AIVR.  ■ 

SELECTED  REFERENCES 

1.  Schamroth  L:  Idioventricular  tachycardia.  / Electrocardiol  1968;1:205-212. 

2.  Rothfeld  EL,  Zucker  IR:  Multiform  accelerated  idioventricular  rhythm. 
Angiology  1974;25:457-461. 

3.  Sclarovsky  S,  Strasberg  B,  Martonovich  G,  et  al:  Ventricular  rhythms  with 
intermediate  rates  in  acute  myocardial  infarct.  Chest  1978;74:180-182. 

4.  Sclarovsky  S.  Strasberg  B,  Fuchs  J,  et  al:  Multiform  accelerated  idioven- 
tricular rhythm  in  acute  myocardial  infarction.  Am  } Cardiol  1983;52:43-47. 


Dr.  Martinez-Lopez  is  a specialist  in  cardiovascular  diseases  affiliated 
with  the  Cardiology  Service,  Department  of  Medicine  at 
William  Beaumont  Army  Medical  Center  in  El  Paso,  TX. 

The  opinions  and  assertions  contained  herein  are  the  private  views  of  the 
author  and  not  to  be  construed  as  official  or  as  reflecting  the  views  of 
the  Department  of  the  Army  or  Department  of  Defense. 


12  JOURNAL  VOL  140  JANUARY 


OTOLARYNGOLOGY/ 

HEAD  & NECK  SURGERY  REPORT 


STRIDOR  IN  INFANTS  AND  CHILDREN 


J.  LINDHE  GUARISCO,  MD;  H.  DEVON  GRAHAM  III,  MD; 

HENRY  A.  MENTZ  III,  MD 


Stridor  is  a sign  of  upper  airway  obstruction. 
Though  it  may  be  associated  with  a benign 
disorder,  it  may  be  the  initial  sign  of  a life- 
threatening  disease.  The  various  congenital  and 
acquired  etiologies  of  stridor  in  infants  and 
children  are  reviewed.  Key  diagnostic  and 
therapeutic  measures  are  briefly  discussed. 


STRIDOR  IS  AiN  abnormally  harsh  respiratory  sound 
of  variable  pitch  produced  by  turbulent  airflow 
through  a partial  obstruction.  It  may  occur  as  a result 
of  obstruction  in  any  portion  of  the  upper  airway. 
Though  stridor  may  be  the  result  of  a relatively  benign 
process,  it  is  often  the  initial  sign  of  a serious  and 
even  life-threatening  disorder.  It  is  the  purpose  of  this 
paper  to  review  some  of  the  more  common  etiologies 
of  upper  airway  obstruction  in  infants  and  children 
and  briefly  outHne  a rational  diagnostic  and  thera- 
peutic approach  to  the  problem. 

ANATOMY 

The  upper  airway  begins  at  the  nares  and  lips  and 
ends  with  the  secondary  bronchi.  It  is  convenient  for 
diagnostic  purposes  to  divide  the  upper  airway  into 
three  different  anatomic  regions.  These  are  the  su- 
praglottic  airway,  the  subglottic-extrathoracic  airway, 
and  the  subglottic-intrathoracic  airway.  The  supra- 
glottic  airway  includes  the  nose,  oral  cavity,  naso- 
pharynx, oropharynx,  hypopharynx,  and  supraglottic 
larynx.  The  subglottic-extrathoracic  airway  includes 
the  glottis  (vocal  cords  and  1 cm  below),  subglottis 
(cricoid  ring),  and  cervical  trachea.  The  subglottic- 


JOURNAL  VOL  140  JANUARY  13 


TABLE  1 

CONGENITAL  ETIOLOGIES 


I.  Anatomic 

1 ) Choanal  atresia 

2)  Micrognathia  (Treacher-Collins) 

3)  Macroglossia  (Beckwith-Wiedemann) 

4)  Thyroglossal  duct  cyst 

5)  Lingual  thyroid 

6)  Laryngomalacia 

7)  Laryngoceles 

8)  Laryngeal  webs 

9)  Vocal  cord  paralysis 

1 0)  Vocal  cord  cysts 

1 1 ) Subglottic  stenosis 

12)  Subglottic  hemangioma 

13)  Vascular  compression  (aberrant  innominate) 

14)  Tracheal  stenosis 

15)  Tracheomalacia 

16)  Esophageal  duplication  cysts 

17)  Bronchial  stenosis 

18)  Bronchogenic  cysts 

19)  Others 

II.  Infectious 

1)  Syphilis 

2)  Herpes 

3)  Others 

III.  Neoplasms 

1)  Teratoma 

2)  Neuroblastoma 

3)  Hemangioma 

4)  A-V  malformations 

5)  Others 

IV.  Neurologic 

1)  CNS  malformation 

2)  Hypoxic  encephalopathy 

3)  Others 


intrathoracic  airway  is  made  up  of  the  intrathoracic 
trachea  and  the  mainstem,  primary  and  secondary 
bronchi.^  By  using  this  anatomic  classification  and  lo- 
calizing the  origins  of  the  stridor  through  careful  his- 
tory and  physical  examination,  the  differential  diag- 
nosis may  be  greatly  narrowed. 

PATHOPHYSIOLOGY 

Stridor  may  be  the  result  of  any  of  four  patho- 
physiologic mechanisms.  Intraluminal  lesions,  extrin- 
sic abnormalities  leading  to  airway  compression,  and 
diseases  leading  to  mucosal  thickening  or  smooth 
muscle  contraction  may  all  result  in  stridor.  In  chil- 
dren minimal  changes  in  airway  diameter  may  lead 

14  JOURNAL  VOL  140  JANUARY 


to  significant  airway  compromise.  This  is  demon- 
strated by  Poiseuille's  law  which,  in  effect,  states  that 
the  resistance  of  the  airway  is  inversely  proportional 
to  the  fourth  power  of  the  radius.  For  example,  if  the 
radius  of  the  airway  is  decreased  by  1 mm  (from  3 
mm  to  2 mm),  a fivefold  increase  in  driving  pressure 
is  necessary  to  maintain  airflow.  As  the  changing 
pressure  increases,  an  additional  physiologic  princi- 
ple, known  as  the  Venturi  principle,  comes  into  play. 
This  states  that  linear  movement  of  a gas  creates  a 
drop  in  pressure  at  a vector  90°  to  the  vector  of  gas 
movement.  Therefore,  in  our  previous  example,  as 
driving  pressure  is  increased,  the  airway  waUs  tend 
to  collapse  inward.^ 

ETIOLOGY 

There  are  numerous  congenital  and  acquired  causes 
of  upper  airway  obstruction.  The  most  common  con- 
genital disorders  leading  to  stridor  are  anatomic  mal- 
formations of  the  upper  airway.  Congenital  infec- 
tions, neoplasms,  and  neurologic  disorders  may  also 
involve  the  upper  airway  and  lead  to  varying  degrees 
of  obstruction.  The  most  common  acquired  etiologies 
of  stridor  are  infectious  diseases.  Other  acquired  etiol- 
ogies include  allergic,  neoplastic,  traumatic,  neuro- 
logic, and  idiopathic  inflammatory  disorders  of  the 
upper  airway.  Tables  1 and  2 list  some  of  the  more 
common  causes  of  congenital  and  acquired  upper  air- 
way obstruction.^'^ 

MANAGEMENT 

The  evaluation  of  a child  with  stridor  should  ob- 
viously begin  with  a careful  history  and  physical  ex- 
amination. Clues  to  specific  congenital  and  acquired 
disorders  are  easily  obtained  with  proper  questioning. 
The  past  medical  history  is  important.  Any  prior  his- 
tory of  intubation,  airway  instrumentation,  or  airway 
trauma  is  especially  relevant.  The  physical  exam 
should  include  a complete  set  of  vital  signs  and  height 
and  weight  measurements.  The  anthropometric 
measurements  are  very  important  in  evaluating  a child 
with  chronic  stridor.  For  example,  a young  child  with 
chronic  low-grade  obstruction  secondary  to  tonsil  and 
adenoid  hypertrophy  with  height  and  weight  in  the 
less  than  fifth  percentile  has  a serious  disorder  re- 
quiring surgical  intervention.  The  nose,  mouth,  oral 
cavity,  nasopharynx,  oropharynx,  hypopharynx,  and 
larynx  must  be  carefully  inspected.  The  flexible  fi- 


beroptic  endoscope  facilitates  an  excellent  office  ex- 
amination of  the  upper  airway  to  the  level  of  the  glot- 
tis. Auscultation  of  the  upper  airway,  as  weU  as  the 
lung  periphery,  will  give  reliable  clues  to  the  site  of 
the  abnormality.  The  remainder  of  the  physical  ex- 
amination must  not  be  neglected  as  valuable  clues  to 
systemic  disease  may  be  overlooked. 

Basic  laboratory  and  radiographic  studies  may  aid 
in  diagnosis.  Lateral  and  AP  neck  films  and  inspira- 
tory and  expiratory  chest  films  may  be  very  useful. 

A complete  blood  count  with  differential  count,  a 
monospot,  Epstein-Barr  virus  titers,  throat  and  blood 
cultures,  and  latex  agglutination  studies  on  blood  and 
urine  may  assist  in  determining  a specific  infectious 
etiology.  Special  laboratory  and  radiographic  tests  are 
ordered  as  necessary.  High  resolution  computed  to- 
mography scanning  and  xeroradiographs  of  the  upper 
airway  are  often  very  helpful.  The  final  step  in  di- 
agnosis is  rigid  endoscopy.  This  is  required  to  verify 
lesions  at  or  below  the  level  of  the  vocal  cords. 

The  most  important  aspect  of  treating  a child  with 
stridor  is  to  ensure  an  adequate  airway.  In  certain 
instances,  emergency  measures  must  be  undertaken 
as  the  initial  phase  of  management  prior  to  complet- 
ing the  history  and  physical.  After  the  airway  has 
been  properly  secured,  additional  therapy  is  insti- 
tuted. Supportive  measures  include  intravenous  fluids, 
humidification,  O2,  suctioning,  proper  positioning, 
and  aerosol  treatments.  Disease  specific  measures  are 
instituted  as  indicated.  Medical  therapy  most  often 
involves  the  use  of  steroids  and  antibiotics.  Medical 
treatment  of  certain  allergic,  neoplastic,  and  idi- 
opathic inflammatory  disorders  usually  requires  the 
expertise  of  the  appropriate  consultant.^ 

Surgical  therapy  may  initially  involve  tracheot- 
omy to  bypass  a life-threatening  obstruction.  Excision 
of  neoplasms,  repair  of  airway  trauma,  reconstruction 
of  the  larynx  and  trachea,  removal  of  foreign  bodies, 
adenotonsiUectomy,  anti-reflux  surgery,  and  other 
procedures  are  recommended  as  indicated. 

SUMMARY 

Stridor,  a sign  of  upper  airway  obstruction,  has  nu- 
merous congenital  and  acquired  etiologies,  many  of 
which  are  life  threatening.  A meticulous  approach  to 
the  history  and  physical  examination,  including  flex- 
ible fiberoptic  endoscopy,  will  facilitate  proper  diag- 
nosis. Basic  and  special  laboratory  tests  are  often  use-  ► 


TABLE  2 

ACQUIRED  ETIOLOGIES 


I.  Infectious 

1)  Purulent  rhinitis 

2)  Ludwig’s  angina 

3)  Tonsillitis 

4)  Peritonsillar  abscess 

5)  Retropharyngeal  abscess 

6)  Epiglottitis 

7)  Laryngotracheobronchitis  (viral  croup) 

8)  Bacterial  tracheitis 

9)  Bacterial  bronchitis 

10)  Viral  bronchitis 

11)  Others 

II.  Allergic 

1)  Allergic  rhinitis 

2)  Hereditary  angioneurotic  edema 

3)  Anaphylaxis 

4)  Others 

III.  Neoplasms 

1)  Papilloma 

2)  Hemangioma 

3)  Lymphangioma 

4)  Lymphoma 

5)  Rhabdomyosarcoma 

6)  Cystic  hygroma 

7)  Others 

IV.  Trauma 

1)  Facial  fractures 

2)  Lingual  hematoma  (hemophiliacs) 

3)  Retropharyngeal  hematoma  (cervical  spine  injury) 

4)  Laryngotracheal  fractures 

5)  Inhalation  or  ingestion  injuries 

6)  Intubation  injury  (subglottic  stenosis,  subglottic 
granuloma) 

7)  Others 

V.  Neurologic  disorders 

1)  Loss  of  innervation  and/or  coordination  of  upper 
aerodigestive  tract  muscles  with  pooling  of 
secretions  and  aspiration 

VI.  Idiopathic  inflammatory 

1)  Wegener’s  granulomatosis 

2)  Relapsing  polychondritis 

3)  Juvenile  rheumatoid  arthritis  (fixation  of  arytenoids) 

4)  Others 

VII.  Others 

1)  Foreign  bodies 

2)  Tonsil  and  adenoid  hypertrophy 

3)  Gastroesophageal  reflux 

4)  Psychogenic 


JOURNAL  VOL  140  JANUARY  15 


ful.  Rigid  endoscopy  is  usually  necessary  to  confirm 
the  diagnosis  if  the  obstruction  is  at  or  below  the  level 
of  the  vocal  cords.  Treatment  includes  proper  sup- 
portive and  disease  specific  measures.  The  most  im- 
portant aspect  of  management  is  the  protection  of  the 
airway.  ■ 


REFERENCES 

1.  Richardson  MA,  Cotton  RJ:  Anatomic  abnormalities  of  the  pediatric  air- 
way. Pediatri  Clin  North  Am  1984;31:821-834. 

2.  Barnes  SD,  Grob  CS,  Lachman  BS,  et  al:  Psychogenic  upper  airway  ob- 
struction presenting  as  refractory  wheezing.  / Pediatr  1986;109:1067-1070. 

3.  Hen  J:  Current  management  of  upper  airway  obstruction.  Pediatr  Ann 
1986;15:274-294. 

4.  Holinger  PH,  Brown  CT:  Congenital  webs,  cysts,  laryngoceles  and  other 
anomalies  of  the  larynx.  Ann  Otol  Rhinol  Laryngol  1967;76:744-752. 

5.  Holinger  LD:  Etiology  of  stridor  in  the  neonate,  infant  and  child.  Ann 
Otol  Rhinol  Laryngol  1980;89:397-400. 

6.  Orenstein  SR,  Orenstein  DM,  Washington  PF,  et  al:  Gastroesophageal 
reflux  causing  stridor.  Chest  1983;84:301-302. 

7.  Rychman  J,  Rodgers  BM:  Obstructive  airway  disease  in  infants  and  chil- 
dren. Surg  Clin  North  Am  1985;65:1663-1687. 


Dr.  Guarisco  is  from  the  Dept  of  Otolaryngology,  Section  on  Pediatric 
Otolaryngology  at  Ochsner  Clinic  and  Alton  Ochsner  Medical 
Foundation  in  New  Orleans.  He  is  also  affiliated  with  the  Dept  of 
Otolaryngology  at  Tulane  Medical  Center  in 

New  Orleans. 

Drs.  Graham  and  Mentz  are  from  the  Dept  of  Otolaryngology  at 
Tulane  Medical  Center  in  New  Orleans. 

Requests  for  reprints  should  be  sent  to  Dr  ].  Lindhe  Guarisco, 
Department  of  Otolaryngology,  Section  on  Pediatric  Otolaryngology, 
Ochsner  Clinic,  1514  Jefferson  Hwy,  New  Orleans,  LA  70121. 


OlRAFATE' 

(sucralfate) 


BRIEF  SUMMARY 


CONTRAINDICATIONS 

There  are  no  known  contraindications  to  the  use  of  sucralfate. 

PRECAUTIONS 

Duodenal  ulcer  is  a chronic,  recurrent  disease.  While  short-term  treatment 
with  sucralfate  can  result  in  complete  healing  of  the  ulcer,  a successful 
course  of  treatment  with  sucralfate  should  not  be  expected  to  alter  the 
post-healing  frequency  or  severity  of  duodenal  ulceration. 

Drug  Interactions:  Animal  studies  have  shown  that  the  simultaneous 
administration  of  CARAFATE  with  tetracycline,  phenytoin,  or  cimetidine  will 
result  in  a statistically  significant  reduction  in  the  bioavailability  of  these 
agents.  This  interaction  appears  to  be  nonsystemic  in  origin,  presumably 
resulting  from  these  agents  being  bound  by  CARAFATE  in  the  gastrointesti- 
nal tract.  The  bioavailability  of  these  agents  may  be  restored  simply  by 
separating  the  administration  of  these  agents  from  that  of  CARAFATE  by 
two  hours.  The  clinical  significance  of  these  animal  studies  is  yet  to  be 
defined. 

Carcinogenesis,  Mutagenesis,  Impairment  of  Fertility:  No  evi- 
dence of  drug-related  tumorigenicity  was  found  in  chronic  oral  toxicity 
studies  of  24  months'  duration  conducted  in  mice  and  rats  at  doses  up  to  1 
gm/kg  (12  times  the  human  dose).  A reproduction  study  in  rats  at  doses  up 
to  38  times  the  human  dose  did  not  reveal  any  indication  of  fertility  impair- 
ment. Mutagenicity  studies  have  not  been  conducted. 

Pregnancy:  Pregnancy  Category  B.  Teratogenicity  studies  have  been 
performed  in  mice,  rats,  and  rabbits  at  doses  up  to  50  times  the  human  dose 
and  have  revealed  no  evidence  of  harm  to  the  fetus  due  to  sucralfate.  There 
are,  however,  no  adequate  and  well-controlled  studies  in  pregnant  women. 
Because  animal  reproduction  studies  are  not  always  predictive  of  human 
response,  this  drug  should  be  used  during  pregnancy  only  if  clearly  needed. 

Nursing  Mothers:  It  is  not  known  whether  this  drug  is  excreted  in 
human  milk.  Because  many  drugs  are  excreted  in  human  milk,  caution 
should  be  exercised  when  sucralfate  is  administered  to  a nursing  woman. 

Pediatric  Use:  Safety  and  effectiveness  in  children  have  not  been 
established. 

ADVERSE  REACTIONS 

Adverse  reactions  to  sucralfate  in  clinical  trials  were  minor  and  only  rarely  led 
to  discontinuation  of  the  drug.  In  studies  involving  over  2,500  patients, 
adverse  effects  were  reported  in  121  (4.7%).  Constipation  was  the  most 
frequent  complaint  (2.2%).  Other  adverse  effects,  reported  in  no  more  than 
one  of  every  350  patients,  were  diarrhea,  nausea,  gastric  discomfort,  indi- 
gestion, dry  mouth,  rash,  pruritus,  back  pain,  dizziness,  sleepiness,  and  vertigo. 

DOSAGE  AND  ADMINISTRATION 

The  recommended  adult  oral  dosage  for  duodenal  ulcer  is  1 gm  four  times  a 
day  on  an  empty  stomach. 

Antacids  may  be  prescribed  as  needed  for  relief  of  pain  but  should  not 
be  taken  within  one-half  hour  before  or  after  sucralfate. 

While  healing  with  sucralfate  may  occur  during  the  first  week  or  two, 
treatment  should  be  continued  for  4 to  8 weeks  unless  healing  has  been 
demonstrated  by  x-ray  or  endoscopic  examination. 

HOW  SUPPLIED 

CARAFATE  (sucralfate)  1-gm  pink  tablets  are  supplied  in  bottles  of  100  and 
in  Unit  Dose  Identification  Paks  of  100.  The  tablets  are  embossed  with 
MARION/1712.  Issued  3/84 

References: 

1.  Korman  MG,  Shaw  RG,  Hansky  J,  et  al:  Gastroenterology  80:1451-1453, 
1981. 

2.  Korman  MG,  Flansky  J,  Merrett  AC,  etal:  D/g  D/s  5c/ 27:71 2-71 5, 1982. 

3.  Brandstaetter  G,  Kratochvil  P:  Am  J Med  79(suppl  2C):36-38, 1985. 

4.  Marks  IN,  Wright  JR  Gilinsky  NH,  et  al:  J Clin  Gastroenterol  8:419-423, 
1986. 

5.  Lam  SK,  Hui  WM,  Lau  WY,  et  al:  Gastroenterology  92:1 193-1201, 1987. 


Another  patient  benefit  product  Irom 

— PHARMACEUTICAL  DIVISION 

MARION 


16  JOURNAL  VOL  140  JANUARY 


1594H7 


When  brain  and  bowel  conflict 


Iflstiitie 

the  Peacemaker. 


In  irritable  bowel  syndrome*  anxiety  can  aggravate  intestinal  symptoms,  which  may 
further  intensify  anxiety  — a distressing  cycle  of  brain/bowel  conflict.  Librax  intervenes  with 
two  well-known  compoimds.  The  Librium®  (chlordiazepoxide  HCl/Roche)  component 
safely  relieves  anxiety.  And  Quarzan®  (cHdinium  bromide/Roche)  provides  antisecretory 
and  antispasmodic  action  to  relieve  discomfort  associated  with  intestinal  hypermotility. 

Dual  action  — for  peace  between  brain  and  bowel.  Because  of  possible  CNS  effects,  caution 
patients  about  engaging  in  activities  requiring  complete  mental  alertness.  Specify  Adjimctive 


LIBR^ 

Each  capsule  contains  5 mg  chlordiazepoxide  HCl 
and  2.5  mg  clidinium  bromide 


*Librax  has  been  evaluated  as  possibly  effective  as  adjunctive  therapy  in  the  treatment  of  peptic  ulcer  and  the  irritable  bowel  syndrome. 
Copyright  © 1987  by  Roche  Products  Inc.  All  rights  reserved.  Please  see  summary  of  prescribing  information  on  adjacent  page. 


CALENDAR 


February 


Febraary  4-6 

Third  International  Conference  on  Monoclonal  Antibody 
Immunoconjugates  for  Cancer,  San  Diego.  Contact:  Office  of 
Continuing  Medical  Education,  M-017,  University  of  California 
San  Diego  School  of  Medicine,  La  Jolla,  CA  92093;  (619)534-3940. 

February  5-8 

Terminal  Care:  Consultations  on  Clinical  and  Policy  Pro- 
blems, Hilton  Head,  South  Carolina.  Penny  B.  Weingarten, 
Program  Coordinator,  Concern  for  Dying,  250  West  57th  St,  Room 
829,  New  York,  NY  10107;  (800)248-2122. 

February  6-13 

Infectious  & Toxicologic  Emergencies,  Snowbird  Resort, 
Snowbird,  Utah.  Contact:  Edith  S.  Bookstein,  Conference 
Management  Associates,  PO  Box  2586,  La  Jolla,  CA  92038; 
(619)454-3212. 

February  9-12 

Update  Yoiu-  Pediatrics-1988,  New  Orleans.  Contact:  J.A. 
D'Angelo  Jr,  Office  of  Continuing  Education,  Tulane  University 
Medical  Center,  1430  Tulane  Ave,  New  Orleans,  LA  70112-2699; 
(504)588-5466. 

February  11-13 

Second  Annual  UCSD-Sharp  Memorial  Hospital  Interna- 
tional Cardiac  Symposium,  San  Diego.  Contact:  Office  of  Con- 
tinuing Medical  Education,  M-017,  Univeristy  of  California  San 
Diego  School  of  Medicine,  La  Jolla,  CA  92093;  (619)534-3940. 

February  11-13 

Vascular  Surgery  Course,  New  Orleans.  Contact:  Alton 
Ochsner  Medical  Foundation,  1516  Jefferson  Hwy,  New  Orleans, 
LA  70121;  (504)838-3702. 

February  11-13 

Mardi  Gras  Endocrinology  Update,  New  Orleans.  Contact: 
Alton  Ochsner  Medical  Foundation,  1516  Jefferson  Hwy,  New 
Orleans,  LA  70121;  (504)838-3702. 

February  13-15 

Mardi  Gras  Anesthesia  Update,  New  Orleans.  Contact:  J.A. 
D'Angelo  Jr,  Office  of  Continuing  Education,  Tulane  University 
Medical  Center,  1430  Tulane  Ave,  New  Orleans,  LA  70112-2699; 
(504)588-5466. 

February  15-17 

Recent  Advances  in  Geriatric  Rehabilitation  1988:  What  Is 


It?  Who  Needs  It?  What  Works?,  San  Diego.  Contact:  Office 
of  Continuing  Medical  Education,  University  of  San  Diego  School 
of  Medicine,  La  Jolla,  CA  92093;  (619)534-3940. 

February  16-21 

The  Fundamentals  of  Plastic  Surgery— The  Basics  in  Perspec- 
tive, Snowbird  Ski  & Summer  Resort,  Snowbird,  Utah.  Con- 
tact: American  Society  of  Plastic  and  Reconstructive  Surgeons,  233 
N Michigan  Ave,  Suite  1900,  Chicago,  IL  60601;  (312)856-1818. 

February  20-22 

New  Orleans  Academy  of  Ophthalmology  37th  Aimual 
Symposium  on  What's  New  in  Ophthalmology,  New 

Orleans.  Contact:  Emily  Busby,  Executive  Secretary,  Eye,  Ear, 
Nose  & Throat  Hospital,  145  Elk  Place,  Room  203,  New  Orleans, 
LA  70112. 

February  20-27 

Duke  at  Vail:  Frontiers  in  Dermatology  and  Rheumatology, 

Vail,  Colorado.  Contact:  Angelika  Langen,  Box  3135,  Duke 
University  Medical  Center,  Durham,  NC  27710;  (919)684-2504. 

February  20-27 

Pediatric  Emergencies,  Royal  Lahaina  Resort,  Maui,  Hawaii. 
Contact:  Edith  S.  Bookstein,  Conference  Management  Associates, 
PO  Box  2586,  La  Jolla,  CA  92038;  (619)454-3212. 

February  22-26 

Physician  in  Management-Seminar  I,  The  Royal  Plaza  at 
Disney  World,  Orlando,  Florida.  Contact:  Sherry  Mason, 
American  Academy  of  Medical  Directors,  4830  W Kennedy  Blvd, 
Suite  648,  Tampa,  FL  33609-2517;  (813)287-2000. 

February  24-26 

Aestetic  and  Reconstructive  Rhinoplasty— What's  New  in 
Plastic  Surgery?,  Manzanillo,  Colima,  Mexico.  Contact:  Juanita 
Navarette,  Division  of  Plastic  & Reconstructive  Surgery,  Har- 
bor/UCLA Medical  Center,  1000  W Carson  St,  Torrance,  CA 
90509;  (213)533-2760. 

February  25-27 

Second  International  Conference  on  Intracavitary 
Chemotherapy,  San  Diego.  Contact:  Office  of  Continuing 
Medical  Education,  M-017,  University  of  California  San  Diego 
School  of  Medicine,  La  Jolla,  CA  92093;  (619)534-3940. 

February  26-27 

Arrhythmias:  Interpretation,  Diagnosis  and  Management, 

New  Orleans.  Contact:  Medical  Education  Resources,  5808  S Rapp 
St,  Suite  202,  Littleton,  CO  80120;  (800)421-3756,  (303)798-9682. 


22  JOURNAL  VOL  140  JANUARY 


February  26-28 

Rhinoplasty:  An  Educational  Symposium,  Dallas.  Contact: 
Continuing  Education,  The  University  of  Texas  Health  Science 
Center  at  Dallas,  5323  Harry  Hines  Blvd,  Dallas,  TX  75235; 
(214)688-2166. 

February  28  - March  4 

Annual  Meeting  of  the  United  States  and  Canadian 
Academy  of  Pathology,  Washington,  DC.  Contact:  Dr.  Nathan 
Kaufman,  Building  C,  Suite  B,  3515  Wheeler  Road,  Augusta,  GA 
30909;  (404)733-7550. 


March 


March  6-11 

9th  Annual  Mammoth  Mountain  Emergency  Medicine, 

Mammoth  Lakes,  California.  Contact:  Medical  Conferences,  Inc, 
CME  Travel  Service,  1615  S Mission  Road,  Suite  3,  Fallbrook,  CA 
92028;  (714)650-4156. 

March  7-9 

j World  Congress  III  on  Cancers  of  the  Skin,  The  Lincoln 
I Hotel  Post  Oak,  Houston.  Contact:  University  of  Texas  M.D. 

I Anderson  Hospital  and  Tumor  Institute,  Office  of  Conference  Ser- 
j vices  HMB  131,  1515  Holcombe  Blvd,  Houston,  TX  77030; 

\ (713)792-2222. 


1988  Annual  Meeting 
Louisiana  State  Medical  Society 
March  10-13,  Lake  Charles 


March  12-27 

Australia/New  Zealand  - Diagnostic  Imaging  Down  Under, 

Australia  and  New  Zealand.  Contact:  Medical  Seminars  Inter- 
national, 21915  Roscoe  Blvd,  Suite  222,  Canoga  Park,  CA  91304; 
(818)719-7380. 

March  14-18 

2nd  Annual  Update  on  Primary  Care,  Steamboat  Springs, 
Colorado.  Contact:  Larry  G.  McLain,  MD,  Dept  of  Pediatrics, 
Loyola  University  Medical  Center,  2160  South  First  Ave, 
Maywood,  Illinois  60153;  (312)531-3195. 


March  16-19 

Highlights  in  Women's  Health  Care,  Orlando,  Horida.  Con- 
tact: Susan  Larson,  Director,  Scott  and  White  Office  of  Continu- 
ing Medical  Education,  2401  South  31st  St,  Temple,  TX  76508; 
(817)774-4083. 

March  17-18 

Assessment  of  Clinical  Competence  in  Specialty  Medicine, 

Toronto  Hilton  Harbour  Castle  Hotel,  Toronto.  Contact: 
American  Board  of  Medical  Specialties,  One  Rotary  Center  #805, 
Evanston,  IL  60201. 

March  17-20 

Hair  Replacement  Surgery,  Los  Angeles.  Contact:  American 
Academy  of  Facial  Plastic  and  Reconstructive  Surgery,  1101  Ver- 
mont Ave  NW,  Suite  404,  Washington,  DC  20005. 


JOURNAL  VOL  140  JANUARY  23 


Sancy  H.  McCool,  LSMSA  President  H 


AUXILIARY  REPORT 


LONG-RANGE  PLANNING 

MARILYN  S.  CANALE 


AS  AN  ADVISORY  COMMITTEE  to  the  Louisiana  State 
Medical  Society  Auxiliary,  the  Long-Range  Plan- 
ning Committee  has  the  duty  to  study  and  evaluate 
present  programs  and  procedures,  and  make  deci- 
sions now  in  order  to  avoid  escalating  problems  that 
will  necessitate  hasty  decisions  in  the  future.  Sec- 
ondly, the  Committee  looks  at  the  future  objectives 
and  growth,  and  developing  programs  and  goals  by 
using  available  resources. 

The  Long-Range  Planning  Committee  must  be 
selected  carefully,  with  consideration  for  continuity 
and  experience.  Two  of  the  current  members.  Opal 
McBride  and  Lorre  Lei  Jackson,  are  former  state  pres- 
idents and  Long-Range  Planning  chairmen.  Christy 
Maraist,  Martha  Maxwell  and  Christy  Owens  were 
selected  for  their  past,  and  current,  involvement  in 
health  and  fund-raising  activities  and  membership. 
The  members  of  the  Committee  are  also  representa- 
tive of  the  entire  membership,  reflecting  all  age  groups 
and  geographical  areas  of  the  state. 

The  first  step  in  long-range  planning  is  to  estab- 
lish an  information  base  of  overall  objectives.  Last 
year's  Committee  evaluated  present  programs  by 
means  of  an  internal  survey  of  each  parish  auxiliary. 

24  JOURNAL  VOL  140  JANUARY 


Every  facet  of  auxiliary  work  and  involvement  was 
covered.  The  internal  analysis  showed  "work,  enthu- 
siasm and  community  involvement  reflecting  a 
strengthening  community  service  organization." 

Change  and  growth  were  evident  in  the  health 
programs.  More  auxiliaries  are  now  addressing  pro- 
grams involving  children,  such  as  child  abuse  pro- 
tection, youth  suicide,  child  care  and  health  and  chil- 
dren health  fairs. 

The  rapport  between  the  state  and  parish  medical 
societies  and  the  state  and  parish  medical  society  aux- 
iliaries has  been  growing  each  year.  Auxilians 
throughout  the  state  respond  to  the  call  for  legislative 
alerts  and  two  auxilians  sit  on  the  board  of  their  parish 
societies.  Programs  for  membership  were  innovative 
and  productive.  Antique  shows,  style  shows,  sharing 
cards  and  a golf  tournament  all  combined  to  raise  over 
$60,000  for  Louisiana  medical  schools. 

The  Long-Range  Planning  Committee,  after  es- 
tablishing the  information  base,  is  now  identifying 
basic  problems  and  opportunities  by  examining  our 
state  administrative  policy  and  functions.  Questions 
and  perceived  problems  have  been  sent  to  the  chair- 
men and  they  are  now  in  the  process  of  being  studied 


and  reviewed  by  the  Committee.  Short-  and  long- 
term objectives  and  programs  are  being  developed. 
Actionable  objectives,  which  are  those  that  we  can  do 
something  about,  include  the  allocation  and  dispo- 
sition of  funds  for  the  Annual  Meeting.  It  has  been 
recognized  that  times  and  circumstances  change,  and 
that  auxiliary  policies  must  be  flexible  enough  to  ac- 
commodate these  changes.  The  Committee  is  also 
evaluating  the  establishment  of  criteria  guidelines  for 
the  selection  of  honored  guests,  guidelines  for  the 
responsibilities  of  the  president  and  president-elect, 
and  the  eligibility  requirements  as  they  are  now  writ- 
ten. Questions  concerning  membership  delegate 
count,  and  the  lack  of  uniformity  among  parish,  state, 
and  national  membership  deadline  dates  are  being 
thoughtfully  and  carefully  studied. 

Recommendations  have  been  made  to  the  Aux- 


iliary to  stimulate  decisions  that  will  contribute  to  the 
growth  of  the  Auxiliary.  The  Long-Range  Planning 
Committee  has  analyzed  where  the  Auxiliary  is  now, 
on  the  parish  level  and,  administratively,  on  the  state 
level.  There  are  short-range  goals  developed  for  the 
coming  year,  and  long-range  goals  for  future  years. 
Some  questions  are  already  answered,  some  solutions 
already  in  place.  Other  questions  have  been  directed 
to  the  Executive  Committee  with  recommendations 
or  will  be  addressed  by  the  serious  effort  of  an  ad  hoc 
committee.  This  is  Long-Range  Planning  — an  on- 
going process  to  fulfill  goals,  present  and  future.  ■ 


Mrs.  Canale  (wife  of  Dr.  Thomas  J.  Canale)  is  chairman  of  the  Long- 
Range  Planning  Committee  of  the  LSMS  Auxiliary. 


Timberlawn  Psychiatric  Hospital 

E.stablished  in  1917 
Children  • Adolescents  • Adults 

• 232  Inpatient  Beds  • Substance  Abuse  Services 

• Outpatient  Services  Inpatient  and  Outpatient  Programs 

• Panial  Hospitalization  Programs  Health  Professionals  Program 

• Residential  Services  Residential  After  Care 

• Departments  of  Psychology,  • Psychiatric  Residency’  Training  Program 

Neuropsychology  and  Social  Work  • Child  Residenq’  Training  Program 

• Family  Assessment  and  Treatment  • JCAH  Approved 

Admissions:  RO.  Box  11288  Dallas,  Texas  75223  214/381-7181 


JOURNAL  VOL  140  JANUARY  25 


ANNOUNCING 


Convenient  500-mg  b.i.d. 
dosage  and  demonstrated 
effectiveness  for 
treatment  of: 

□ skin  and  skin  structure  infections* 

□ uncomplicated  cystitis^ 

□ pharyngitis* 


• New  hydrochloride  salt  form  of  cephalexin— 
requires  no  conversion  in  the  stomach  before 
absorption 

• Well-tolerated  therapy 

• May  be  taken  without  regard  to  meals 

For  other  indicated  infections,  250-mg  tablets  available 
for q. id.  dosage 


Priced  less  than  Keflex®cephaiexin) 


Keftab  is  contraindicated  in  patients  with  known  allergy  to  the 
cephalosporins  and  should  be  given  cautiously  to  penicillin- 
sensitive  patients. 

Penicillin  is  the  drug  of  choice  in  the  treatment  and  prevention 
of  streptococcal  infections,  including  the  prophylaxis 
of  rheumatic  fever. 


KEFTAB™ 

(cephalexin  hydrochloride  monohydrate) 

Summary:  Consult  the  package  literature  for 
prescribing  information. 

Indications  and  Usage: 

Respiratory  tract  infections  caused  by  susceptible 
strains  of  Streptococcus  pneumoniae  and  group  A 
iS-hemolytic  streptococci. 

Skin  and  skin  structure  infections  caused  by  sus- 
ceptible strains  of  Staphylococcus  aureus  and/or 
jS-hemolytic  streptococci. 

Bone  infections  caused  by  susceptible  strains  of 
S aureus  and/or  Proteus  mirabilis. 

Genitourinary  tract  infections,  including  acute  prosr 
tatitis,  caused  by  susceptible  strains  of  Escherichia 
coli,  P mirabilis,  and  Klebsiella  sp. 

Contraindication:  Known  allergy  to  cephalosporins. 

Warnings:  KEFTAB  SHOULD  BE  ADMINISTERED 
CAUTIOUSLY  TO  PENICILLIN-SENSITIVE  PA- 
TIENTS. PENICILLINS  AND  CEPHALOSPORINS 
SHOW  PARTIAL  CROSS-ALLERGENICITY.  POSSI- 
BLE REACTIONS  INCLUDE  ANAPHYLAXIS. 
Administer  cautiously  to  allergic  patients. 
Pseudomembranous  colitis  has  been  reported  with 
virtually  all  broad-spectrum  antibiotics.  It  must  be 
considered  in  differential  diagnosis  of  antibiotic- 
associated  diarrhea.  Colon  flora  is  altered  by  broad- 
spectrum  antibiotic  treatment,  possibly  resulting  in 
antibiotic-associated  colitis. 

Precautions: 

• Discontinue  Keftab  in  the  event  of  allergic  reac- 
tions to  it. 

• Prolonged  use  may  result  in  overgrowth  of  nonsus- 
ceptible  organisms. 

• Positive  direct  Coombs'  tests  have  been  reported 
during  treatment  with  cephalosporins. 

• Keftab  should  be  administered  cautiously  in  the 
presence  of  markedly  impaired  renal  function.  Al- 
though dosage  adjustments  in  moderate  to  severe 
renal  impairment  are  usually  not  required,  careful 
clinical  observation  and  laboratory  studies  should 
be  made. 

• Broad-spectrum  antibiotics  should  be  prescribed 
with  caution  in  individuals  with  a history  of  gas- 
trointestinal disease,  particularly  colitis. 

• Safety  and  effectiveness  have  not  been  determined 
in  pregnancy  and  lactation.  Cephalexin  is  excreted 
in  mother’s  milk.  Exercise  caution  in  prescribing 
Keftab  for  these  patients. 

• Safety  and  effectiveness  in  children  have  not  been 
established. 

Adverse  Reactions: 

• Gastrointestinal,  including  diarrhea  and,  rarely,  nau- 
sea and  vomiting.  Transient  hepatitis  and  chole- 
static jaundice  have  been  reported  rarely. 

• Hypersensitivity  \n  the  form  of  rash,  urticaria,  angio- 
edema,  and,  rarely,  erythema  multiforme,  Stevens- 
Johnson  syndrome,  or  toxic  epidermal  necrolysis. 

• Anaphylaxis  has  been  reported. 

• Other  reactions  have  included  genital/anal  pruri- 
tus, genital  moniliasis,  vaginitis/vaginal  discharge, 
dizziness,  fatigue,  headache,  eosinophilia,  neutro- 
penia, and  thrombocytopenia;  reversible  interstitial 
nephritis  has  been  reported  rarely. 

• Cephalosporins  have  been  implicated  in  trigger- 
ing seizures,  particularly  in  patients  with  renal 
impairment. 

• Abnormalities  in  laboratory  test  results  included 
slight  elevations  in  aspartate  aminotransferase 
(AST,  SCOT)  and  alanine  aminotransferase  (ALT, 
SGPT).  False-positive  reactions  for  glucose  in  the 
urine  may  occur  with  Benedict’s  or  Fehling’s  solu- 
tion and  Clinitest®  tablets  but  not  with  Tes-Tape® 
(Glucose  Enzymatic  Test  Strip,  USP,  Lilly). 


"'Due  to  susceptible  strains  of  Staphylococcus  aureus  and/or  /3-hemolytic  streptococci. 
■ Due  to  susceptible  strains  of  Escherichia  coli,  Proteus  mirabilis.  and  Klebsiella  sp, 

’ Due  to  susceptible  strains  of  group  A /3-hemolytic  streptococci. 


PV  2060  DPP  [091887] 


849336 


TRAUMATIC  OCCUPATIONAL 
OCCLUSIVE  ARTERIAL  DISEASE 
OF  THE  HANDS 


TERRY  R.  JONES,  MD;  JOHN  D.  FRUSHA,  MD; 
JON  V.  SCHELLACK,  MD 


28  JOURNAL  VOL  140  JANUARY 


Hypothenar  hammer  syndrome  occurs  following 
ulnar  artery  occlusion  or  aneurysm  formation 
resulting  from  repetitively  using  the  hypothenar 
area  of  the  hand  to  hammer,  strike,  push,  or  twist 
hard  objects.  Vibration  syndrome  occurs  from  the 
use  of  vibrating  tools  and  results  in  Raynaud's 
phenomenon  or  even  digital  gangrene.  Although 
the  hypothenar  hammer  syndrome  and  the 
vibration  syndrome  are  not  well  publicized,  they 
have  important  implications  to  vocational 
disability.  A case  report  is  presented  and  the 

syndromes  discussed. 

PATIENTS  WITH  unilateral  upper  extremity  ischemia 
or  Raynaud's  phenomenon  should  have  a careful 
history  and  physical  to  determine  if  their  arterial  prob- 
lem may  be  related  to  occupational  trauma.  Failure  to 
discover  this  possibility  may  deprive  patients  of  right- 
ful disability  compensation  or  result  in  less  than  op- 
timal medical  management. 

We  have  treated  several  patients  with  occupa- 
tion-caused ischemia  of  the  upper  extremity  and  have 
found  that  some  insurance  companies  were  unfamil- 
iar with  these  syndromes.  In  one  current  textbook, 
devoted  entirely  to  upper  extremity  vascular  disor- 
ders, less  than  a single  paragraph  is  devoted  to  hy- 
pothenar hammer  syndrome,^  and  in  one  review  of 
500  articles  in  the  world  literature  on  vibration  syn- 
drome, only  15  were  in  the  American  literature.^  We 
present  a case  which  illustrates  both  these  conditions. 

CASE  REPORT 

A 53-year-old  right-handed  white  male  electrician  de- 
veloped pain,  paresthesias,  and  discoloration  of  his 
right  hand  several  hours  after  using  it  to  repeatedly 
slam  conduit  pipe  across  a box  in  an  effort  to  bend 
the  pipe.  His  work  also  involved  daily  use  of  a vi- 
brating tool  called  a rotary  hammer,  and  he  admitted 
using  his  hand  regularly  to  strike  objects.  He  sought 
medical  attention  several  days  later  and  was  started 
I on  nifedipine.  Ischemic  signs  and  symptoms  pro- 
j grossed  and  he  was  referred  for  vascular  surgery  eval- 
uation. 

Physical  examination  disclosed  bluish  mottling  of 
i the  hypothenar  eminence  of  the  hand  and  obvious 
ischemia  of  digits  2-5  but  no  apparent  abnormality  of 
his  thumb.  A transfemoral  arch  aortogram  and  selec- 


Fig  1.  Arteriogram  showing  occlusion  of  most  of 
the  superficiai  and  deep  paimer  arterial 
arches. 


tive  brachial  arteriogram  (Fig  1)  was  done;  demon- 
strated was  occlusion  of  the  distal  ulnar  artery  and 
the  superficial  palmar  arch.  The  patient  underwent 
streptokinase  therapy  with  subsequent  clearing  of  the 
mottling  of  his  hypothenar  eminence  and  restoration 
of  carpal  arch  blood  flow.  His  digital  flow  was  im- 
proved but  ischemia  persisted.  He  was  started  on 
dextran,  nifedipine,  and  pentoxifylline,  with  further 
improvement.  He  was  discharged  on  aspirin,  nifed- 
ipine, and  pentoxifylline.  Several  weeks  later  his  hand 
appeared  normal.  The  nifedipine  and  pentoxifylline 
were  tapered  and  discontinued  with  no  exacerbation 
of  ischemic  signs  or  symptoms.  Nine  months  later, 
on  a follow-up  visit,  he  complained  of  cold  sensitivity 
in  his  right  hand  and  reported  temporary  paresthesias 
when  he  tried  to  use  a hammer.  He  was  considered 
totally  disabled  to  perform  his  usual  work  and  a vo- 
cation change  was  recommended. 

DISCUSSION 

The  term  "hypothenar  hammer  syndrome"  was  first 
used  by  Conn,  et  al  in  1970  to  describe  the  ulnar  artery 
occlusion  that  resulted  from  repetitive  blunt  trauma 
to  the  hand.^  Individuals  using  the  hypothenar  area 
of  their  hand  to  hammer,  strike,  push,  or  twist  hard 
objects  can  injure  the  ulnar  artery  against  the  hook 
of  the  hamate  wrist  bone  (Fig  2).  The  syndrome  has  ► 

JOURNAL  VOL  140  JANUARY  29 


Fig  2.  Diagram  iiiustrating  how  uinar  artery  may  be 
impacted  against  hook  of  hamate  carpai  bone 
from  direct  pressure  to  hypothenar  emin- 
ence of  the  hand. 


a high  incidence  in  auto  mechanics  and  electricians 
but  can  occur  in  any  situation  in  which  the  hand  is 
misused,  such  as  by  devotees  of  the  martial  arts  and 
by  patients  who  lean  on  canes  or  crutches. 

This  syndrome  probably  occurs  more  frequently 
than  is  reported  due  to  the  reluctance  of  patients  to 
seek  medical  assistance  for  a problem  that  threatens 
termination  of  their  jobs.  In  one  survey  of  127  vehicle 
maintenance  workers,  79  admitted  to  using  their  hands 
as  a hammer  on  a regular  basis.  Eleven  of  these  79 


men  (14%)  exhibited  signs  and  symptoms  of  the  hy- 
pothenar hammer  syndrome,  and  yet  they  had  not 
sought  medical  attention.^ 

Other  reasons  for  the  failure  to  recognize  this 
syndrome  are  the  apparent  triviality  of  the  respon- 
sible injury  or  misdiagnosis  of  the  condition.^  The 
differential  diagnosis  includes  Raynaud's  disease, 
Raynaud's  phenomenon  associated  with  connective 
tissue  disease,  direct  trauma  to  the  fingers,  ischemia 
from  emboli  secondary  to  proximal  disease,  primary 
occlusive  vascular  disease,  chemical  poisonings,  dys- 
globulinemias,  blood  dyscrasias,  and  neurologic 
causes. 

The  symptoms  may  be  quite  variable,  producing 
from  no  symptoms  or  just  intermittent  paresthesias 
to  the  full  clinical  picture  of  Raynaud's  phenomenon 
or  gangrene.  One  reason  for  the  variability  of  symp- 
toms is  the  variability  in  the  anatomy  of  the  normal 
hand.  The  ulnar  artery  usually  terminates  as  the  su- 
perficial palmar  arch  from  which  the  palmar  digital 
arteries  arise.  However,  this  arch  is  complete  in  only 
70%  of  individuals.®'  ^ Although  the  fourth  and  fifth 
digits  are  most  commonly  involved  in  hypothenar 
hammer  syndrome  (HHS),  any  digit  can  be  involved 
because  of  this  variability  in  blood  supply. 

The  diagnosis  of  HHS  can  be  strongly  suspected 
when  Raynaud's  phenomenon  appears  in  the  domi- 
nant hand  of  a male  worker  who  has  used  his  hands 
repetitively  to  strike  hard  objects.  In  one  large  series 
of  966  patients  with  Raynaud's  phenomenon,  there 
was  a 1.7%  incidence  of  HHS.®  The  syndrome  occurs 
rarely  in  women.  It  can  occur  bilaterally.  Occasionally 
the  ulnar  artery  injury  will  result  in  an  aneurysm  which 
can  be  palpatead  as  a pulsatile  mass  near  the  wrist. 
If  the  aneurysm  has  thrombosed,  the  mass  must  be 
differentiated  from  ganglion  cyst  or  tumor.  Usually, 
HHS  does  not  involve  the  thumb  and  does  not  exhibit 
neurological  symptoms  or  hyperemia. Arteriog- 
raphy is  required  for  definitive  diagnosis,  to  exclude 
other  disease,  and  to  delineate  the  anatomy  and  ex- 
tent of  involvement  so  that  an  adequate  treatment 
plan  may  be  formulated. 

Treatment  consists  of  resection  of  the  ulnar  artery 
aneurysm,  if  present,  and  reconstruction  of  the  ulnar 
artery.  If  no  aneurysm  is  present,  conservative  man- 
agement is  recommended  since  the  prognosis  is  ex- 
cellent once  the  causative  trauma  has  been  discontin- 
ued. 

Vibration  syndrome  is  a term  used  to  describe 


30  JOURNAL  VOL  140  JANUARY 


the  symptoms  of  Raynaud's  phenomenon  in  workers 
who  use  vibrating  tools  and  who  have  no  other  etiol- 
ogy for  the  phenomenon.  The  syndrome  is  known 
variously  as  Raynaud's  phenomenon  of  occupational 
origin,  vibration-induced  white  finger,  traumatic 
vasospastic  disease,  dead  finger,  and  dead  hand.^  Un- 
like HHS,  vibrating  syndrome  may  exhibit  neurolog- 
ical symptoms  or  produce  orthopedic  complications 
such  as  osteoarthritis  at  the  wrist  or  shoulders,  carpal 
bone  cysts,  or  olecranon  exostoses. 

The  incidence  and  recognition  of  vibratory  syn- 
drome is  greater  than  that  of  the  HHS.  In  one  survey, 
the  vibration  syndrome  was  shown  to  occur  to  some 
degree  in  89%  of  American  stonecutters^^  and,  in  an- 
other survey,  in  79%  of  shipyard  caulkers. The  vi- 
bration syndrome  also  has  a high  incidence  in  forest 
workers  who  use  chain  saws,  although  improve- 
ments in  chain  saw  design  have  dramatically  reduced 
the  incidence. 

The  pathogenesis  of  the  vibration  syndrome  is 
unclear  but  has  been  shown  to  correlate  with  the  du- 
ration of  exposure  and  the  physical  character  of  the 
vibration:  different  frequencies  and  amplitudes  pre- 
dispose either  to  the  osteoarticular  lesions  or  to  neu- 
rovascular manifestations.^^'  The  effects  of  exposure 
to  vibrations  are  also  influenced  by  ergonomic  factors, 
eg,  how  the  tool  is  handled,  and  biological  suscep- 
tibility. Since  vibration  syndrome  seems  to  pref- 
erentially involve  the  ulnar  artery,  as  does  the  HHS, 
i it  is  not  clear  in  the  present  case  study  which  source 
of  trauma  was  more  causative  of  the  hand  ischemia. 

HHS  and  vibration  syndrome  are  uncommon  but 
important  causes  of  Raynaud's  phenomenon.  Both 
syndromes  are  usually  reversible  if  treated  early  and 
appropriately.  Diagnosis  is  important  for  proper  treat- 
ment, vocational  counseling,  and  initiating  disability 
claims.  Although  known  for  many  years,  these  syn- 
■ dromes  have  not  received  wide  publication  in  Amer- 
ican medical  literature  and  may  be  more  prevalent 
than  commonly  realized.  ■ 

REFERENCES 

1.  Machleder  HL:  Vascular  Disorders  of  the  Upper  Extremity.  Mount  Kisco, 
New  York,  Futura  Publishing  Co,  Inc,  1983. 

2.  Behrens  V,  Wasserman  D,  Carlson  W,  et  al;  Vibration  syndrome  in 
chipping  and  grinding  workers.  / Occup  Med  1984;26:765-788. 

3.  Conn  J Jr.,  Bergan  JJ,  BeU  JC:  Hypothenar  hammer  syndrome:  Post- 
traumatic  digital  ischemia.  Surgery  i970;68:1122-1128. 

4.  Pineda  CJ,  Weisman  MH,  Bookstein  JJ,  et  al:  Hypothenar  hammer  syn- 
drome: Form  of  reversible  Raynaud's  phenomenon.  Amer  } Med 
1985;79:561-570. 


5.  Vayssairat  M,  Debure  C,  Cormier  J,  et  al:  Hypothenar  hammer  syn- 
drome: Seventeen  cases  with  long  term  foUow  up.  J Vase  Surg  1987;5:838- 
843. 

6.  Wasserman  DE:  Raynaud's  phenomenon  as  it  relates  to  hand-tool  vi- 
bration in  the  workplace.  Am  bid  Hyg  Assoc  J 1985;46:10-14. 

7.  Little  JM,  Ferguson  DA:  The  incidence  of  the  hypothenar  hammer  syn- 
drome. Arch  Surg  1972;105:684-685. 

8.  Calenoff  L:  Angiography  of  the  hand:  Guidelines  for  interpretation.  Ra- 
diology 1972;102:331-335. 

9.  Coleman  SS,  Anson  BJ:  Arterial  patterns  in  the  hand  based  upon  a study 
of  650  specimens.  Surg  Gynec  Obstet  1961;113:409-424. 

10.  Benedict  KT,  Chang  W,  McCready  FJ:  The  hypothenar  hammer  syn- 
drome. Radiology  1974;111:57-60. 

11.  Taylor  W,  Wasserman  D,  Behrens  V,  et  al:  Effect  of  the  air  hammer  on 
the  hands  of  stonecutters.  The  limestone  quarries  of  Bedford,  Indiana, 
revisited.  Brit  J bit  Med  1984;41:289-295. 

12.  Bovenzi  M,  Petronio  L,  DiMarino  F:  Epidemiological  survey  of  shipyard 
workers  exposed  to  hand-arm  vibration.  Int  Arch  Occup  Environ  Health 
1980;46:251-266. 

13.  Miyashita  K,  Shiomi  S,  Itoh  N,  et  al:  Epidemiological  study  of  vibration 
syndrome  in  response  to  total  hand-tool  operating  time.  Br  } Ind  Med 
1983;40:92-98. 

14.  Starck  J:  FEgh  impulse  acceleration  levels  in  hand-held  vibrating  tools. 
An  additional  factor  to  the  hazards  associated  with  the  hand-arm  vibra- 
tion syndrome.  Scand  J Worl  Environ  Health  1984;10:171-178. 

15.  Lee  EH,  Evans  JG:  Vibration-induced  white  finger  disease:  a case  report. 
Can  J Surg  1984;27:513-514. 


Drs.  Jones  and  Frusha  are  clinical  assistant  professors  in  the  Dept  of 
Surgery  at  LSU  School  of  Medicine  in  Baton  Rouge. 

Dr.  Schellack  is  a clinical  instructor  in  the  Dept  of  Surgery  at  LSU 

School  of  Medicine  in  Baton  Rouge. 

All  three  authors  are  also  engaged  in  group  private  practice  limited  to 

vascular  surgery  in  Baton  Rouge. 

Reprint  requests  should  be  sent  to  Terry  R.  Jones,  MD, 
5329  Didesse  Dr,  Baton  Rouge,  LA  70808;  (504)769-4493. 


JOURNAL  VOL  140  JANUARY  31 


Physicians  Recognition  Award 

Twenty-six  physicians  from  the  state  of  Louisiana  were  awarded  the  Physicians  Recognition  Award  [PRA]  during 
October,  1987.  This  award  is  presented  by  the  American  Medical  Association  to  physicians  who  have  voluntarily 
completed  1 50  hours  of  continuing  medical  education  during  a consecutive  three-year  time  period.  Of  these  1 50 
hours,  at  least  60  must  be  in  AMA/PRA  Category  1.  These  twenty-six  individuals  are  presented  below. 


Baton  Rouge 

Metairie 

Frank  Maurer  Buckingham,  MD 
Richard  Hugh  Gold,  MD 
Gregory  Orlando  Harrison  MD* 

Charles  Joseph  Cucchiara,  Jr.,  MD 
Michael  D.  Horowitz,  MD* 

Chalmette 

Michael  Sydney  Ellis,  MD 

Monroe 

Felix  Jefferson  Willey,  MD 

Jennings 

Scott  Blume  Gremillion,  MD 

New  Iberia 

David  E.  Bourgeois,  MD 

Kenner 

Khalil  Yousef  Imsais,  MD 

New  Orleans 

Philip  V.  Beilina,  Jr.,  MD 
Theodore  Joseph  Borgman,  MD 
Robert  McMurtry  Gilliland,  III,  MD 

Lafayette 

Joan  S.  Grode  Milner,  MD 
P.  Safari-Kermanshahi,  MD 

Ernest  Joseph  Kaminski,  MD 
Abner  Martin  Landry,  Jr.,  MD 
Gordon  Lee  Love,  MD* 

Lake  Charles 

Thomas  Paul  Alderson,  MD 

David  Anthony  Newsome,  MD* 
Carlos  Alberto  Trujillo,  MD 
Robert  Franklin  Wood,  MD 

Marksville 

Fernando  Garcia  Garcia,  MD 

Ruston 

Nur  Badshah,  MD* 

Marrero 

Martin  James  O'Neill,  Jr.,  MD 

Winnsboro 

Elvin  Gregory  Tubre,  MD 

* These  individuals  are  not  members  of  the  Louisiana  State  Medical  Society 


32  JOURNAL  VOL  140  JANUARY 


A CASE  OF  METASTATIC  CARCINOMA 
IN  ASSOCIATION  WITH 
PAGET’S  DISEASE  OF  BONE 


DAVID  J.  HOLCOMBE,  MD 


A previously  healthy,  65-year-old  black  man  was 
diagnosed  as  having  wide  spread  Paget's  disease  of 
bone  with  a large  lytic  lesion  in  the  right  femur. 
Curettage  with  prophylactic  insertion  of  a rod  was 
performed  and  the  surgical  specimen  tentatively 
identified  as  sarcoma.  Subsequent  computed 
tomography  scan  of  the  abdomen  identified  a left 
suprarenal  mass  which  was  determined,  from 
percutaneous  biopsy,  to  be  a spindle  cell  renal 
carcinoma  similar  histologically  to  the  lytic  lesion 
in  the  right  femur.  Any  uncertainty  as  to  the 
sarcomatous  nature  of  tumors  arising  in  pagetic 
bone  should  evoke  the  possibility  of  carconima  of 

metastatic  origin. 


SPORADIC  REPORTS  of  the  association  between  met- 
astatic carcinoma  and  Paget's  disease  of  the  bone 
have  been  published. This  rare  association  has  been 
attributed  to  the  predilection  of  pagetic  bone  to  met- 
astatic seeding  due  to  hypervascularization. ^ In  all  of 
these  previous  cases,  the  confirmation  of  metastatic 
carcinoma  was  made  with  biopsy.  Unfortunately,  the 
histological  picture  may  not  always  be  clear-cut.  Since 
sarcomatous  degeneration  has  been  reported  to  occur 
in  27%  of  patients  older  than  40  suffering  from  Paget's 
disease,^  the  diagnosis  of  osteosarcoma  in  the  pres- 
ence of  a lytic  lesion  seems  the  most  likely  one^  in  the 
absence  of  any  other  observed  tumor.  Given  the  his- 
tological variation  in  sarcomas,^  the  possibility  of  met- 
astatic carcinoma  must,  however,  be  considered  when 
the  pathological  findings  appear  sufficiently  atypical. 
In  the  case  presented  here,  an  initial  tentative  diag- 
nosis of  sarcoma  was  later  modified  to  metastatic  car- 
cinoma when  the  presumed  primary  was  located. 

A 65-year-old  black  man  with  no  significant  past 
medical  history  came  to  the  emergency  room  three 
times  in  one  month  with  a chief  complaint  of  right 
thigh  pain.  He  claimed  to  have  been  well  until  five 
years  prior  to  admission  when  he  began  having  slight, 

JOURNAL  VOL  140  JANUARY  37 


Fig  1 . Radiograph  of  pelvis  and  proximal  femur  re- 
vealing extensive  pagetic  changes  as  well 
as  lytic  lesion  of  right  proximal  femur. 


intermittent,  right  upper  thigh  discomfort.  During  the 
preceding  month,  the  pain  had  grown  progressively 
worse  and  now  was  a dull  ache,  exacerbated  by  weight 
bearing  as  well  as  by  pushing  on  the  brake  pedal  of 
his  car.  The  pain  was  slightly  relieved  by  rest  and  did 
not  waken  him  from  sleep.  He  denied  any  fever,  chills, 
anorexia,  or  weight  loss.  He  had  been  treated  symp- 
tomatically with  indomethacin,  which  had  alleviated 
the  pain  but  did  not  eliminate  it.  At  his  last  emergency 
room  visit,  x-rays  of  the  right  hip  and  femur  were 
performed  and  revealed  marked  cortical  thickening 
of  both  bones  compatible  with  Paget's  disease  and, 
in  addition,  a large  lucency  in  the  proximal  femur 
eroding  the  cortex  (Fig  1). 

The  patient  had  no  allergies  and  was  taking  only 

38  JOURNAL  VOL  140  JANUARY 


indomethacin  (25  mg  tid)  as  prescribed  on  a previous 
emergency  room  visit.  He  was  a retired  truck  driver, 
now  working  as  a school  bus  driver.  He  had  smoked 
one  pack  per  day  for  15  years  and  had  drunk  six  cans 
of  beer  a day  for  10  years.  Family  history  and  review 
of  systems  were  noncontributory.  The  patient's  blood 
pressure  was  120/80,  his  heart  rate  80/min,  and  his 
temperature  97°  F.  Physical  examination  was  remark- 
able only  for  pain  on  compression  of  the  upper  right 
femur  and  for  some  fine  disseminated  inspiratory  and 
expiratory  crackles  in  both  lung  fields.  Laboratory  ex- 
aminations were  remarkable  for  a normochromic, 
normocytic  anemia  (hemoglobin  8.9  g/dL  and  he- 
matocrit 27%),  a platelet  count  of  566,000,  an  elevated 
alkaline  phosphatase  of  205  U/L,  and  a sedimentation 
rate  of  62  mm/h.  Urinalysis  was  negative.  Later,  a 24- 
hour  hydroxproline  urinary  excretion  test  proved  to 
be  elevated  at  110  mg/24  h.  Chest  x-rays  showed 
chronic  lung  disease  with  diffuse  interstitial  fibrosis 
and  focal  fibrosis  of  the  right  perihilar  region,  and 
focal  fibrosis  or  infiltrate  of  the  right  perihilar  region. 
The  ECG  on  admission  was  normal. 

Subsequent  bone  scan  and  skeletal  survey  re- 
vealed the  presence  of  wide-spread  pagetic  involve- 
ment of  the  right  femur,  right  hip,  left  femur,  right 
tibia,  both  humeri,  several  vertebrae,  and  a right  rib 
posteriorly.  The  patient  underwent  surgical  curettage 
of  the  lytic  lesion  of  the  right  femur  and  insertion  of 
a metallic  intramedually  rod  as  prophylaxis  against 
pathological  fracture.  The  surgical  specimen  was  ex- 
amined and  reported  to  be  consistent  with  sarcoma, 
with  some  reservation  as  to  its  exact  characteristics 
due  to  the  absence  of  osteoid  bone  (Fig  2). 

In  order  to  exclude  the  presence  of  lung  metas- 
tases  from  the  presumed  sarcoma,  not  evident  on  the 
routine  chest  films,  the  patient  was  sent  for  a com- 
puted tomography  CT  scan  of  the  lung  which  showed 
a possible  left  upper  lobe  infiltrate  as  well  as  the  pos- 
sibility of  very  small  bilateral  effusions.  At  that  time, 
an  abdominal  CT  scan  was  included  because  of  the 
suggestion  of  a left  adrenal  tumor.  This  CT  scan  dem- 
onstrated the  presence  of  nonenhancing  left  supra- 
renal and  right  renal  masses,  previously  unsuspected. 
The  left  suprarenal  mass  underwent  percutaneous  bi- 
opsy with  a tentative  diagnosis  of  carcinoma,  prob- 
ably renal,  with  spindle  cell  characteristics  similar  to 
those  previously  identified  as  fibrosarcoma  in  the  lytic 
lesion  of  the  right  femur  (Fig  3).  The  diagnosis  was 


Fig  2.  Photomicrograph  of  bone  biopsy  from  right 
proximal  femur,  initially  diagnosed  as  sar- 
coma. 


thus  retrospectively  transformed  from  one  of  sarcoma 
arising  out  of  pagetic  bone  to  one  of  metastatic  seed- 
ing of  carcinoma  into  pagetic  bone. 

The  patient  underwent  radiotherapy  to  the  right 
femur  with  excellent  symptomatic  relief.  Unfortu- 
nately, he  was  readmitted  two  and  a half  months  after 
his  initial  hospitalization  with  complaints  of  increas- 
ing weakness  and  shortness  of  breath.  He  died  shortly 
afterwards;  subsequent  autopsy  confirmed  the  pres- 
ence of  a large  hypernephroma  of  the  right  kidney 
with  a metastatic  lesion  in  the  contralateral  adrenal 
gland.  In  addition,  disseminated  metastatic  lesions 
were  identified  in  both  striated  and  cardiac  muscle, 
partially  explaining  his  global  weakness,  dyspnea,  and 
late  cardiac  conduction  problems.  These  widespread 
metastatic  lesions  were  uniformly  less  than  1 cm  in 
diameter,  most  of  them  being  considerably  smaller. 

This  case  represents  one  of  six  reported  in  the 
literature  of  metastatic  carcinoma  associated  with  Pa- 
get's disease  of  bone.  The  possibility  of  such  a diag- 
nosis should  be  kept  in  mind,  especially  if  the  his- 
tological diagnosis  of  presumed  osteosarcoma  appears 
at  all  uncertain.  ■ 

REFERENCES 

1.  Castleman  B and  McNeill  M:  Case  records  of  the  Massachusetts  General 
Hospital;  weekly  clinicopathological  exercise  42292.  N Engl  } Med 
1956;255:145. 


Fig  3.  Photomicrograph  of  suprarenal  percuta- 
neous biopsy  specimen  consistent  with 
carcinoma  of  kidney. 


2.  Agha  FP,  Norman  A,  Hirschl  S,  et  al:  Paget's  disease.  Coexistence  with 
metastatic  carcinoma.  NY  State  J Med  1976;76:734-735. 

3.  Kahnowski  DT,  Goodwin  CA:  Case  Report  179:  Metastic  disease  devel- 
oping in  Paget  disease  of  bone  in  the  distal  end  of  femur.  Skeletal  Radiol 
1981;7:229-231. 

4.  Hermann  G,  Szpom  A,  Schwarts  I,  et  al:  Metastatic  carcinoma  involving 
Paget  disease  of  the  bone:  An  unusual  association.  Mt  Sinai  ] Med 
1983;50(6):537-539. 

5.  Powell  N:  Metastatic  carcinoma  in  association  with  Paget's  disease  of 
bone.  Br  J Radiol  1983;56:582-585. 

6.  Huvos  AG,  Butler  A,  Bretsky  SS:  Osteogenic  sarcoma  associated  with 
Paget's  disease  of  the  bone.  Cancer  1983;52:1489-1495. 

7.  Smith  J,  Botet  JF,  Yeh  SDJ:  Bone  sarcomas  in  Paget's  disease:  A study  of 
85  patients.  Radiology  1984;152:583-590. 

ACKNOWLEDGMENTS 

I would  Hke  to  acknowledge  the  helpful  assistance  of 
Miss  Denise  Ardoin  in  preparation  of  this  manuscript. 


Dr.  Holcombe  is  an  internist  affiliated  with  Freedman  Clinic  of  Internal 

Medicine  in  Alexandria. 

Reprints  will  not  be  available. 


JOURNAL  VOL  140  JANUARY  39 


'AIAA  Uli^U 


A SPECIAL 
PRACTICE 
FOR  SPECIALISTS. 


If  you're  a Surgeon  or  OB/GYN  or  Other  Medical  Specialist, 

the  Air  Force  may  hove  a special  practice  tor  you.  What 
makes  it  special?  You'll  enjoy  an  excellent  pay  and  benefits 
package,  There'll  be  more  time  to  spend  with  your  family. 
You'll  receive  30  days  of  vacation  with  pay  each  year.  And 
you  will  work  with  modern  ecjuipment  and  some  of  the  most 
highly  trained  professionals  in  the  world,  serving  your  country 
and  your  patients.  Nowthafs  special!  Find  out  just  how 
special  your  practice  can  be.  Call 


Southern  Louisiana 
504-586-8317  coiiect 


Northern  Louisiana 
817-640-6469  collect 


“DO  YOU  KNOW  A PSYCHIATRIC  CENTER 
WHERE  MY  CHILD  CAN  BE  TREATED?” 


Referring  a family  to  a psychiatric  hospital  for  their 
child’s  treatment  can  he  a difficult  decision  for  any 
physician.  At  River  Oaks,  our  staff  understands  the 
special  needs  of  both  the  patient  and  the  family  in 
coping  with  mental  illness,  behavior  problems,  and 
ennitional  disorders.  River  Oaks  — a private, 
126'hed  facility,  offers  a broad  range  of  programs  for 
the  individual. 

Long  Term  Care 
Appropriate  Medication 
Crisis  Center 
Expressive  Arts 
Outpatient  Clinic 
Substance  Abuse  Program 
information  on  clinical 


Evaluation 

Children 

Adolescents 

Adults 

Accredited  School 

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For  more 


services, 


admission  or  referral,  contact  the  Admissions 
Department,  call  us  collect  at  (504)  734-1740; 
Crisis  Center,  call  733-CARE;  Outpatient  Clinic 
733-5591. 


OAKS 


RIVER  OAKS  PSYCHIATRIC  CENTER 

1525  River  Oaks  Road  West  John  A.  Stocks,  M.D. 

New  Orleans,  LA  70123  Medical  Director 

(504)  734-1740 

THE  NEW  ORLEANS  CENTER  FOR  PSYCHOTHERAPEUTIC  MEDICINE 


Gregory  P.  Roth  William  R.  Sorum,  M.D. 

Managing  Director  Clinical  Director 


A Universal  Health  Services  Facility 


A COMMUNITY  MEDICINE  PROGRAM 
IN  JAMAICA  FOR  FOURTH  YEAR 
MEDICAL  STUDENTS 


IRWIN  COHEN,  MD 


For  two  years,  the  Program  in  Community 
Medicine  of  the  Tulane  University  School  of 
Medicine  has  been  sending  fourth  year  medical 
students  to  serve  six  to  eight  weeks  continuous 
rotations  in  rural  health  enters  in  Cornwall 
County,  Jamaica.  Forty-nine  students  have  gone 
and  38  are  scheduled  for  this  year.  The  students 
live  in  private  homes  and,  assuming  the  duties  of 
a physician,  become  integrated  members  of  rural, 
district  health  care  teams.  The  objectives  of  the 
program  are  to  1)  nurture  humanism,  2)  improve 
history  taking  and  physical  examination  skills,  3) 
promote  interest  in  primary  health  care, 
community  medicine,  and  the  health  team 
approach  to  medical  services,  4)  supplement  health 
manpower  in  Jamaica,  5)  develop  interest  in 
developing-country  work,  and  6)  develop  a 
universal  perspective  of  life  in  the  young 
physician.  Because  the  program  is  the  result  of  an 
agreement  between  a U.S.  medical  school  and  a 
foreign  government,  is  prearranged  for  the 
student,  and  provides  for  a continuous  student 
presence  at  the  foreign  sites,  it  may  well  be  a 
unique  feature  of  Tulane's  medical  curriculum. 


There  are  very  few,  if  any,  medical  school-based 
programs  which  regularly  provide  for  a develop- 
ing-country clerkship  for  undergraduate  medical  stu- 
dents.^ There  is  no  U.S.  literature,  except  for  personal 
testimonies,  documenting  the  effect  of  these  experi- 
ences on  physicains  and  medical  students.^  I believe 
the  effects  can  be  multiple  and  salutary. 

Two-thirds  of  the  American  public  now  believe 
that  people  are  beginning  to  lose  faith  in  doctors.^ 
Patients  assume  that  their  physician  is  competent,  but 
they  also  strongly  desire  integrity,  warmth,  compas- 
sion, attentiveness,  effective  communication,  and  en- 
couragement from  their  physicians.  These  qualities 
and  skills  are  rarely  nurtured  in  the  science-laden  un- 
dergraduate medical  curriculum.  It  is  our  belief  that 
medical  students  will  recognize  the  role  of  humanism 
in  medicine  if  they  are  placed  in  a setting  where  there 
is  a dearth  of  modern  medical  support  facilities,  where 
they  will  live  where  they  work,  and  where  they  will 
view  their  patients  against  the  background  of  their 
homes  and  communities.  Hopefully,  these  experi- 
ences will  be  remembered  and  will  be  used  after  they 
return  to  improve  patient  relationships  and  the  public 
image  of  physicians. 

JOURNAL  VOL  140  JANUARY  41 


Reductions  in  the  cost  of  heath  care 
can  be  accomplished  slowly  by  modi- 
fying medical  curricula  and  de-empha- 
sizing  expensive  technology.  The  proc- 
ess can  be  accelerated,  however,  by 
immersing  medical  students  in  resource- 
poor  environments  where  they  will  dis- 
cover that  good  patient  histories  and 
careful  examinations  are  their  most  pow- 
erful diagnostic  tools. 


Medical  education  in  the  United  States  empha- 
sizes scientific  procedures  and  state-of-the-art  tech- 
nology. Impressive  twentieth  century  advances  in  the 
ability  to  manipulate  biological  systems  foster  phy- 
sician dependence  on  expensive  laboratory  proce- 
dures and  curative  medicine.  However,  health  care 
now  consumes  about  10%  of  the  gross  national  prod- 
uct; 40%  of  this  health  care  share  is  publicly  funded. 
Physicians,  because  they  control  about  70%  of  na- 
tional health  spending,  are  being  asked  to  develop 
more  cost-effective  methods  of  patient  management.^ 
Reductions  in  the  cost  of  health  care  can  be  accom- 
plished slowly  by  modifying  medical  curricula  and 
de-emphasizing  expensive  technology.  The  process 
can  be  accelerated,  however,  by  immersing  medical 
students  in  resource-poor  environments  where  they 
will  discover  that  good  patient  histories  and  careful 
examinations  are  their  most  powerful  diagnostic  tools. 
This  approach,  when  applied  later  in  their  medical 
practices,  can  lead  to  a reduction  in  the  total  cost  of 
health  care. 

As  public  health  care  funds  diminish,  the  im- 
portance of  using  them  efficiently  increases.  The 
amount  apportioned  for  the  primary  care  of  patients 
will  compete  with  that  used  for  community  health 
problems.  By  fusing  primary  health  care  with  com- 
munity medicine  and  by  rendering  the  service  through 
physician-led  health  teams,  a broader  view  of  soci- 
ety's needs  can  be  achieved.  Although  the  decisions 
will  not  be  easier,  they  will  be  more  accurate.^  Such 
a dual  focus  is  characteristic  of  the  system  in  many 
developing  countries.^  A combined  approach,  stress- 
ing both  community  health  promotion  and  current 
technology,  is  long  overdue  in  this  country.  Ironi- 
cally, the  United  States  can  look  to  developing  coun- 
tries for  new  approaches  to  cost-effective  health  serv- 
ices. 

Jamaica  has  a small  national  budget,  of  which  an 
inadequate  amount  is  apportioned  to  health  care  serv- 
ices.^ The  small  numbers  of  health  care  personnel  re- 
flect this.  Physicians  are  in  extremely  short  supply, 
and  this  problem  is  worsening.  The  United  States  has 
an  abundance  of  physicians.  Many  are  unaware  of 
overseas  health  care  problems.  Surely,  we  can  (and 
it  is  possible  to  mount  a moral  argument  that  we 
should)  encourage  our  physicians,  perhaps  either  early 
or  late  in  their  careers,  to  provide  service  to  the  people 
of  these  nations.®  This  type  of  program  will  provide 


42  JOURNAL  VOL  140  JANUARY 


some  immediate  relief  to  the  people  of  Jamaica. 

Opportunities  to  experience  other  health  care 
systems  should  be  offered  by  all  medical  schools,  al- 
lowing nascent  physicians  to  make  more  valid  judg- 
ments about  components  of  their  own  system.  And 
in  this  instance,  because  Jamaica  is  resource-poor,  be- 
cause it  has  a decentralized  and  integrated  primary 
care  and  community  medicine  system,  and  because 
it  renders  service  through  health  care  teams,  under- 
graduate medical  students  can  gain  valuable  insights 
about  the  humanistic  and  cost-control  aspects  of  med- 
icine. 

Therefore,  this  program  is  an  attempt  to:  1)  nu- 
ture  in  young  physicians  feelings  of  humanism  and 
respect  for  the  patient's  dignity,  2)  improve  history 
taking  and  physical  examination  skills  in  a resource- 
poor  setting  to  promote  cost-effective  health  care,  3) 
promote  interest  in  primary  health  care,  community 
medicine  and  the  health  team  approach  to  medical 
services,  4)  supplement  manpower-poor  health  care 
services  in  Jamaica,  5)  stimulate  interest  in  develop- 
ing-country  medical  work,  and  6)  develop  in  the  nas- 
cent physician  a universal  perspective  of  life  so  nec- 
essary to  an  educated  person. 

PROGRAM  DESIGN 

Fourth  year  medical  students  from  Tulane  University 
and  other  U.S.  medical  schools  elect  to  spend  from 
six  to  eight  weeks  living  and  working  in  Jamaica.  They 
live  with  Jamaican  families  in  rural  areas  and  are  at- 
tached to  rural  health  care  teams.  Seven  groups  of 
five  students  are  successively  and  continuously  sent 
to  the  island. 

Before  departure,  the  students  receive  a brief  ori- 
entation to  Jamaica,  a Jamaica  manual  containing  in- 
formation collated  from  reports  concerning  island  life 
submitted  by  past  students,  and  a commercially  pro- 
duced guide  to  Jamaica.  After  arrival,  they  are  ori- 
ented by  the  supervising  Jamaican  staff  in  Montego 
Bay.  The  students  then  are  transported  to  their  rural 
sites. 

The  sites,  unfortunately,  vary  from  session  to  ses- 
sion depending  on  the  availability  of  private  home 
accommodations.  The  sites  used  thus  far  are  Fal- 
mouth, Adelphi,  Cambridge,  Maroon  Town,  Hope- 
well,  Sandy  Bay,  and  Lucea,  all  on  the  western  end 
of  the  island  in  the  parishes  of  Trelawny,  St.  James 
and  Hanover. 


Duties  are  determined  by  the  activities  of  the  dis- 
trict health  care  teams  and  the  parish  health  depart- 
ments. They  include  medical,  pediatric,  obstetric  and 
gynecologic  clinics  at  large  and  small  outreach  facil- 
ities, home  visits,  lectures  to  primary  and  secondary 
schools,  churches  and  health-oriented  community 
groups,  and  visits  to  private  and  public  commercial 
facilities  with  public  health  inspectors.  They  provide 
service  to  a clinic  treating  sexually  transmitted  dis- 
eases, an  old  age  home,  and  an  orphanage  in  Montego 
Bay.  The  students  can  arrange  to  spend  time  in  the 
Casualty  Department  or  on  in-patient  services  at 
Cornwall  Regional  Hospital. 

They  are  required  to  spend  one  week  in  Kingston 
with  the  Department  of  Social  and  Preventive  Med- 
icine at  the  University  of  the  West  Indies.  They  live 
in  the  homes  of  professors,  visit  the  outreach  facilities 
of  this  large,  metropolitan  area  and  take  classes  with 
and  meet  Jamaican  medical  students. 

They  are  also  required  to  formulate  and  conduct 
an  epidemiologic  project.  The  data  are  organized  into 
a written  report  and  are  presented  at  an  end-of-the- 
year  seminar.  The  studies  are  then  combined  in  the 
form  of  a report  to  the  Cornwall  County  Public  Health 
Department. 

The  entire  cost  of  the  trip  ($800  to  $1000)  is  borne 
by  the  student.  Humanitarian  discounts  for  air  travel 
have  been  generously  granted  by  Eastern  and  Air 
Jamaica  Airlines. 

RESULTS 

During  the  first  two  years,  49  students  (43  from  Tu- 
lane Medical  School)  and  three  residents  (from  pe- 
diatric and  family  practice  residencies)  worked  in  Ja- 
maica. This  year  38  students  are  scheduled  (34  from 
Tulane).  The  latter  group  of  students  is  not  discussed 
in  this  report. 

Twenty-six  of  the  Tulane  medical  students  were 
men.  This  reflects  exactly  the  percentage  of  men  in 
this  year's  graduating  class.  The  students  averaged 
2.0  high  passes  per  person  (Tulane's  highest  grade) 
in  their  third  year  clinical  clerkships.  The  entire  grad- 
uating class  averaged  1.9  per  person.  Eighteen  stu- 
dents planned  to  do  residencies  in  internal  medicine, 
nine  in  surgery,  six  in  pediatrics,  and  six  in  obstetrics 
and  gynecology.  Only  two  planned  to  enter  family 
practice  residencies.  Except  for  surgery,  a greater  per- 
centage of  this  group  is  entering  graduate  training  in 

JOURNAL  VOL  140  JANUARY  43 


each  of  the  above  disciplines  when  compared  to  the 
entire  graduating  class.  Nine  students  planned  to 
practice  general  internal  medicine,  six  some  form  of 
surgery,  six  pediatrics,  and  six  obstetrics  and  gyne- 
cology. Only  one  student  indicated  a preference  for 
each  of  family  practice,  public  health,  and  third  world 
medicine.  Twenty-three  students  indicated  they  were 
going  to  establish  a private  practice  while  18  were 
planning  to  enter  academia. 

Before  leaving,  multiple  reasons  were  usually 
given  by  the  students  for  wanting  to  take  this  elective. 
Thirty-five  students  indicated  that  they  wanted  to  ex- 
perience Third  World  medicine.  Thirteen  felt  the  ex- 
perience would  improve  their  clinical  skills  in  am- 
bulatory medicine.  Seven  felt  they  wanted  to  make  a 
contribution  to  humanity  and  seven  chose  reasons  of 
convenience  (cost,  English  is  spoken,  the  trip  was 
organized). 

After  returning,  each  student  listed  multiple  ben- 
efits they  derived  from  the  program.  Forty  felt  that 
they  improved  their  ambulatory  clinical  skills  and  were 
more  confident  in  using  them.  Six  specifically  men- 
tioned how  the  unavailability  of  laboratory  studies 
enhanced  this  effect.  Twenty-seven  were  impressed 
by  the  cultural  differences  they  experienced.  Twenty- 
six  used  the  opportunity  to  compare  our  medical  care 
system  with  that  in  Jamaica.  Fourteen  appreciated  the 
increased  independence  and  responsibility  they  were 
given  and  six  felt  they  became  better-educated  per- 
sons. 

In  assessing  the  program,  18  used  the  word  “ex- 
cellent"; others  called  the  program  "fantastic,"  "mag- 
nificent," "extremely  valuable";  one  student  felt  this 
"was  the  best  cUnical  course"  she  took  and  two  wanted 
to  go  again. 

On  the  other  hand,  seven  students  felt  the  need 
for  better  on-site  supervision  and  orientation  sessions 
and  three  felt  that  a laboratory  and  library  at  the  rural 
sites  were  essential. 

I have  had  two  conferences  with  Jamaican  health 
care  workers  about  student  performance.  Praise  of 
their  medical  knowledge  and  enthusiasm  was  uni- 
versal. Everyone  thought  that  the  program  should 
continue. 

DISCUSSION 

Jamaica  was  chosen  as  the  country  for  this  student 
program  for  the  following  reasons:  it  is  close  to  the 

44  JOURNAL  VOL  140  JANUARY 


United  States  mainland  (making  travel  cheaper),  it  is  | 
a safe  environment  for  expatriate  health  care  workers,  ^ 
the  students  can  live  in  the  community  where  they 
work,  English  is  the  language,  the  people  are  in  need, 
there  is  an  existing,  but  poorly-financed  primary  health 
care  community  medicine  infrastructure,  there  is  an 
established  medical  school,  and  I know  many  of  the 
people  who  organize  health  care  delivery  on  the  is- 
land. 

In  answer  to  the  few  criticisms  made  by  the  stu- 
dents and  the  Jamaican  staff,  the  program  will  now 
begin  with  an  expanded  one  and  one-half  hour  ori-  ; 
entation  session  at  Tulane  University.  Field  supervi- 
sion and  in-country  orientation  sessions  will  be  pro- 
vided by  a Jamaican  physician  who  will  be  hired  by  j 
Tulane  University.  He  will  meet  the  students  at  the 
airport,  inform  them  of  the  nature  of  the  Jamaican 
health  care  system,  medical  personnel,  local  services, 
available  medicines,  living  conditions,  the  trip  to 
Kingston,  the  epidemiologic  project,  and  how  the  stu- 
dents may  integrate  with  Jamaican  rural  health  care  , 
work  and  life.  Libraries  are  being  slowly  created  with 
discarded  medical  texts  by  students.  The  availability 
of  laboratory  services  is  the  responsibility  of  the  host 
country.  The  recurring  costs  of  such  services  preclude 
their  funding  by  this  program.  Furthermore,  it  is  their 
absence  which  makes  Jamaica  a desirable  site. 

The  students  who  selected  the  program  were  a 
reflection  of  the  graduating  class  with  regard  to  sex 
and  clinical  grades  distribution.  A greater  percentage 
of  the  program  group  is  entering  the  graduate  training 
programs  of  the  primary  care  disciplines.  This  was 
especially  evident  in  medicine  (29%  versus  42%).  As 
a consequence,  surgical  training  programs  are  un- 
derrepresented in  the  Jamaica  group  (29%  versus  21%). 

It  is  tempting  to  believe  that  this  elective,  being  an 
ambulatory,  general  practice  experience,  can  serve  as 
a marker  for  those  students  who  wiU  choose  work  in 
a primary  care,  private  practice  setting.  However,  42% 
of  this  group  also  plans  to  enter  academia. 

This  is  a preliminary  report.  Whether  this  pro- 
gram can  achieve  all  its  objectives  is  unknown.  At 
present,  the  students  do  help  to  alleviate  Jamaica's 
health  care  manpower  shortages  and  Jamaican  health 
care  workers  have  repeatedly  told  me  of  their  effec- 
tiveness. 

The  effect  of  the  experience  on  the  students  is 
only  suggested  by  their  comments.  Almost  all  appre- 


dated  the  opportunity  to  practice  and  refine  their  clin- 
ical sldlls,  and  a few  mentioned  how  the  resource- 
poor  environment  facilitated  this  objective.  Whether 
this  appredation  translates  into  less  reliance  on  ex- 
pensive technology  as  sldlls  mature  is  unknown. 

Perhaps  because  students  Uved  in  private  homes 
in  the  communities  where  they  worked  and  met  and 
studied  with  Jamaican  medical  students,  most  were 
impressed  by  the  cultural  differences  of  our  two  so- 
deties  and  by  the  differences  in  our  health  care  de- 
livery systems.  The  experiential  nature  of  this  knowl- 
edge may  strongly  influence  future  activity  in  primary 
health  care,  community  medicine,  or  developing 
country  medical  work.  One  student,  after  returing, 
did  state  that  he  was  now  planning  to  work  in  de- 
veloping countries,  and  five  became  more  aware  of 
the  health  needs  of  the  poor  and  how  local  access 
solves  one  of  those  needs. 

Sadly,  no  one  specifically  mentioned  the  human- 
ism of  the  enterprise;  the  opportunity  to  see  the  effect 
of  illness  and  physician  recommendations  on  patients 
in  their  homes  and  communities.  Only  two  students 
reflected  on  their  place  in  the  world  and  on  the  char- 
acteristics of  a well-rounded  person.  Perhaps  this  is 
because  medical  schools  train  doctors,  they  do  not 
educate  them.  The  training  leaves  the  neophyte  only 
with  the  knowledge  that  powerful  curative  medical 
tools  exist,  but  without  a knowledge  of  how  to  use 
them.  Without  exposure  to  the  humanities,  they  are 
left  without  a broad  view  of  humanity  and  the  uni- 
verse and  without  a tempering  kernel  of  humility.  It 
is,  in  part,  humility  which  prompts  us  to  accept  the 
reality  of  being  a part  of  the  inhumanity  and  human 
tragedy  which  surrounds  us,  and  yet  not  to  forget 
that  with  our  special  sldlls  we  can  be  powerful  actors 
in  the  struggle  to  bring  about  a particle  of  social  jus- 
tice. If  medical  curricula  cannot  include  the  human- 
ities, then  immerse  the  medical  student  in  the  world 
— not  in  the  hospital.  There  he  wiU  learn  of  the  po- 
tential the  practice  of  medicine  holds  for  continuous 
professional  satisfaction. 

Student  and  staff  feedback  suggest  that,  in  the 
short  run,  the  program  is  a success.  Its  potential  value 
in  shaping  desirable  characteristics  in  developing 
physicians  can  only  be  revealed  by  a prospective  study 
of  the  future  professional  activities  of  today's  Jamaica 
influenced  students.  ■ 


l\/l  edical  schools  train  doctors,  they  do 
not  educate  them.  The  training  leaves  the 
neophyte  only  with  the  knowledge  that 
powerful  curative  medical  tools  exist,  but 
without  a knowledge  of  how  to  use  them. 
Without  exposure  to  the  humanities,  they 
are  left  without  a broad  view  of  human- 
ity and  the  universe  and  without  a tem- 
pering kernel  of  humility.  ...  If  med- 
ical curricula  cannot  include  the  human- 
ities, then  immerse  the  medical  student 
in  the  world  — not  in  the  hospital. 


ACKNOWLEDGMENTS 

Without  the  diligent,  voluntary  efforts  of  Dr.  Marjorie 
Holding,  Senior  Medical  Officer  (Health),  Cornwall 
County;  Dr.  SheHa  Campbell,  Medical  Officer  (Health), 
St.  James  Parish;  and  Dr.  Denise  Eldemire,  Depart- 
ment of  Social  and  Preventive  Medicine,  University 
of  the  West  Indies,  this  program  would  not  have  been 
possible. 

REFERENCES 

1.  Baker  TD,  Quinlv  JC:  A U.S.  International  Health  Service  Corps.  JAMA 
1987;257:2622-2625. 

2.  Gorton  MM:  Hospital  practice  in  Nepal.  N Engl  J Med  1985;312:249-250. 

3.  Mechanic  D:  Public  perceptions  of  medicine.  N Engl  J Med  1985;312:181- 
183. 

4.  Spivey  BE:  The  relation  between  hospital  management  and  medical  staff 
imder  a prospective  payment  system.  N Engl  J Med  1984;310:984-986. 

5.  Nutting  PA:  Community  oriented  primar}'  care:  A promising  innovation 
in  primary  care.  Public  Health  Rep  1985;100:3-4. 

6.  Second  Population  Project,  Jamaica,  1976-1980.  Ministry  of  Health  and  En- 
vironmental Control,  Government  of  Jamaica,  1976. 

7.  Pocketbook  of  Statistics.  Jamaica,  Statistical  Institute  of  Jamaica,  1983. 

8.  Pust  RE:  U.S.  abundance  of  physicians  and  international  health.  JAMA 
1984;252:385-388. 


Dr.  Cohen  is  from  the  Program  in  Community  Medicine  at  Tulane 
University  School  of  Medicine  in  New  Orleans. 

Reprints  will  not  be  available. 


JOURNAL  VOL  140  JANUARY  47 


PROFESSIONAL  LISTINGS 


THE  FERTILITY  INSTITUTE  OF  NEW  ORLEANS 

(A  Professional  Corporation) 

Richard  P.  Dickey,  MD,  PhD 

Diplomate,  American  Board  of 
Reproductive  Medicine 
Diplomate,  American  Board  of 
Obstetrics  and  Gynecology 

David  N.  Curole,  MD  Phillip  H.  Rye,  MD  Terry  Olar,  PhD 

Diplomate,  American  Board  Diplomate,  American  Board  Director,  InVitro  Laboratory 

of  Obstetrics  and  Gynecology  of  Obstetrics  and  Gynecology  Member,  Society  for  the 

Study  of  Reproduction 

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AND  OTHER  INFERTILITY  THERAPY  INCLUDING: 

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48  JOURNAL  VOL  140  JANUARY 


JOURNAL 

OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY  February  1988 


Micromrgery  1987:  The  tSU  experience 


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JOURNAL 

OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY  1988 


VOLUME  140  / NUMBER  2 / FEBRUARY 


ARTICLES 


8 

Blood  pressure  control 
in  children 

James  W.  Wade,  MD 
Roy  F.  Brabham,  MD 
L.  Franklyn  Elliott,  MD 

24 

Microsurgery  1987: 
The  LSU  experience 

Krishna  Gravois,  MD 

31 

Sonographic  evaluation 
of  acute  bacterial 

meningitis 

Bruce  A.  Baethge,  MD 
Robert  E.  Wolf,  MD,  PhD 

35 

Gold-induced 

pneumonitis 

DEPARTMENTS 


2 

Information  for  Authors 

3 

New  Members 

11 

ECG  of  the  Month 

16 

Otolaryngology/Head  & 
Neck  Surgery  Report 

22 

Calendar 

43 

Classified  Advertising 

44 

Books  Received 

Cover  illustration  by  Eugene  New,  New  Orleans. 


INFORMATION  FOR  AUTHORS 


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dc'sign.ilc'  one*  .lullior  .is  c orrc'sponcleni  .ind  inc  luclc*  liis/lic*r  .idcirc'ss 
.incI  Ic'Ic'plionc'  number.  M.inusc  ripis  .irc“  rc'cc'ivc'd  wilb  llie  c'xplic  il 
unde'isl.inding  lli.il  llic>y  li.ivc'  nol  bc'c'ii  prc'viously  publislic'cl  .ind  ,ire 
nol  under  c onsicler.ilion  by  .iiiy  ollic'f  public  .ilion.  M.inusc  ri|)ls  ,ire  sub- 
)C'C  I lo  c'clilori.il  revisions  .is  clec*mc‘d  nc*c  c'ss.iry  by  llic*  c'clilors  .iiicl  lo 
such  modilic  .ilions  .is  lo  bring  lliem  iiilo  conforniily  wilb  jouunai. 
slylc*.  Sl.ilemc'iils  m.iclc*  or  opinions  exprc'ssc'cl  by  .iiiy  coniribulor  in 
.iiiy  .irlie  lc“  or  Ic'.ilurc*  publislic'cl  in  llic>  jouhnai,  .ire  tlu'  sole*  respon- 
sibilily  ol  llie  .lullior. 

RFVIEWINCi  PROCIESS.  I .ic  li  m.inusc  ripl  is  rc‘viewc*d  by  llic*  f clilor 
.ind  by  .i  mc*mber(s)  of  llic*  I clilori.il  Bo.ircl  or  llie  I’.inc’l  ol  ( oiisull.inis 
Ironi  whom  l<nowlc*clgc*.iblc*  opinions  .irc*  souglil.  I he*  .ic  c c'pl.ibilily  of 
.1  111. iiiiisc  ripl  is  de'lc'iniinc'd  by  such  f.ic  lots  .is  llie  cjii.ilily  ol  llic* 
111. muse  ripl,  pc*rc  c*ivc*cl  inlc*rc*sl  lo  jouunai.  rc*.iclc*rs,  usc*fulnc*ss  or  im- 
porl.incc*  lo  physic  i. ins,  .ind  llic*  currc*nl  b.icklog  of  .icc  c*plc*d 

m. inusc  ripis.  Aulliors  .irc*  nolilic*d  upon  rc*c  c*ipl  of  llic*  m.inusc  ripl.  Wlic*n 
.IC  c c*pl.ibilily  is  clc*lc*rminc*cl,  .lulliors  will  llic*ii  be*  rc*c|uc*slc*cl  lo  sign  <i 
m.inusc  ripl  c onsc*nl  loriii  Ir.insfc'rring  c opyriglil  privilc*gc*s  lo  llic*  jouu- 
nai.. Ac  c c*plc*cl  m.inusc  ripis  bc*c  onic*  llic*  propc*rly  of  llic*  jouunai,  <incl 
ni.iy  nol  be*  publislic*cl  c*lsc*wlic*rc*,  in  p.iil  or  in  whole*,  willioul  pc*rmis- 
sion  from  llic*  jouunai,.  Absir.ic  is  ni.iy  be*  rc*procluc  c*cl  willioul  spc*c  ific 
pc*rniission,  proviclc*cl  .ic  knc)wlc*clgc*nic*nl  of  llic*  source*  is  m.iclc*. 

TITl.E  PACiE  should  c <iriy  1 1 1 llic*  lillc*  of  llic*  m.inusc  ripl,  wliic  li  should 
be*  c one  isc*  bul  iniorni.ilivc*;  |21  full  ii.inic*  of  c*,u  li  .lullior,  wilb  liiglic'sl 
.1C  .iclc*niic  clc*grc*e*(s),  lisic'cl  in  clc*sc  c*ncling  orclc*r  of  m.igiiilucic*  of  c cin- 
Iribiilion  (only  llic*  n.imc's  of  lliosc*  who  li.ive*  c oiilribulc*d  ni.ilc*ri.illy 
lo  llic*  prc*p.ii. Ilion  of  llic*  m.inusc  ripl  should  be*  inc  luclc*cl);  | f|  ,i  onc*- 
lo  lwo-sc*nlc*nc  c*  biogr.i|)liic  <il  clc*sc  lijilion  for  c*.ic  li  .lullioi  wliic  li  should 
inc  luclc*  spc*c  i.illy,  pi.ic  lie  c*  loc  .ilion,  .ic  .iclc*niic  <ippoinlnic*nls,  prim.iry 
lios|)il.il  .iliili. Ilion,  or  ollic*r  c rc*clils  (.i  pic  lure*,  bl.ic  k-.ind-wliilc*  lic*.icl 
sliol,  of  c*.ic  11  .lullioi  ni.iy  <ilso  be*  sc*iil  if  .iv.iil.ibic*);  |4|  n.imc*  .ind  .icl- 
clic*ss  ol  .lullior  lo  whom  rc*c|uc*sls  for  rc'prinis  should  be*  .iclclrc*ssecl, 
or  .1  sl,ilc*nie*nl  ih.il  rc*priiils  will  nol  be*  .iv.iil.ibic*. 

ABSTRACT  should  be*  on  llic*  sc*c oiicl  ji.igc*  .ind  c onsisi  of  no  more*  ih.in 
ISO  words.  Il  is  clc*sigiic'd  lo  .icciu.iini  ihc*  polc*nli.il  rc*.idc*r  wilh  ihc* 
i*ssc*nc  c*  of  ihc*  lc*xl  .iiicl  should  be*  inform.ilivc*  r.ilhc*r  ih.in  desc  riplivc*. 
(Avoid  lc*lling  wh.il  "will  be*  cic'sc  ribc*cl"  .ind  insic'.icl  clc*sc  ribc*  il.)  The* 
.ibsir.ic  I should  be*  inlc*lligiblc*  whc*n  divorc  c*c!  from  ihc*  .irlic  Ic*,  clc*voicl 
ol  unclc*finc*cl  .ibbrc*vi. ilions,  .iiicl  suil.ibic*,  willioul  rc*wriling,  for 
rc*produc  lion  by  .ibsir.ie  ling  sc*rvic  c*s.  I he*  .ilisir.u  I should  c onl.iiii:  1 1 1 
.1  briel  sl.ilc*mc*nl  ol  ihc*  m.inusc  rijil's  purpose*;  (2|  ihc*  .ijipro.ic  h usc'cl; 

I l|  ihc*  m.ilc'ii.il  sluclic*cl;  |4|  llic*  rc*sulls  c)bl.iinc*cl.  I iiiph.isi/c*  iic'w  .ind 
impoil.iiil  ,ispc*c  Is  oi  ihc*  slucly  or  obsei'v.ilions. 


KEY  WORDS  sfiould  follow  ihe  .ibslrncl  .ind  be*  idc*ntified  as  such. 
I'rovidc*  lhrc*c*  lo  five*  kc*y  words  or  short  jihr.isc's  that  will  assist  index- 
c*rs  in  c ross-indc*xing  your  .irlic  Ic*.  Use*  lc*rms  from  the  Medic  al  Sub- 
jc*cl  llc*.iding  list  from  lnclc*x  Mc*dicus  when  jiossifile. 

SUBHEADS  .irc*  strongly  c*iic  ouragc*d.  They  should  jirovidc*  guidanc  e 
for  ihc*  rc*.iclc*r  .me)  s(*rvc*  lo  fire.ik  the*  tyjiograjihic  monotony  of  the 
lc*xl.  Ihc*  formal  is  flc*xiblc*  but  subheads  cirdinarily  inc  lude*:  Methods 
.md  M.ilc*ri.ils,  C.isc*  Kc*j)orls,  Synijiloms,  Examination,  Trc*alment  and 
lc*(  hnic)uc*,  Kc*sulls,  Discussion,  and  Summary. 

REEERENCES  must  fic*  cloublc*-st).ic  c*cJ  on  a s(*j)arate  shc*et  of  jiajic'r  and 
limilc*d  lo  .1  rc*.ison.i/i/c*  numbc*r.  Tlic*y  will  fie  critically  examinc*ci  al 
llic*  lime*  of  rc*vic*w  .md  must  fic*  kejil  to  a minimum.  All  references 
must  lie*  c ilc*cl  in  ihc*  lc*xl  and  ihc*  list  should  fic*  arrangc*cl  in  order  of 
c il.ilion,  nol  alpli.ific*tic  .illy.  Pc*rscin.il  ccimmunic  ations  and  unpufilishc‘d 
cl.il.i  sfiould  nol  fic*  inc  luc)c*d  in  rc*fc*rc*nces,  but  shoulcf  fic*  inc orporalc^d 
in  ihc*  lc*xl.  flic*  following  form  sfiould  lie*  fcillciwc*d: 

lOUKNAl.S 

1 1 1 Author(s):  Use*  the*  surname*  fcillowe*d  liy  initials  without  jiunctua- 
lion,  flic*  ii.ime*s  of  .ill  .lulhors  should  fic*  give*n  unless  there  are  more 
than  lhrc*c*,  in  which  case*  the*  name's  of  the  first  thre*e*  authors  are 
usc*d,  followc'd  by  "e*l  al."  |2)  Title  of  article.  Cajiitali/e  only  the  first 
lc*tte*r  of  Ihc*  first  word.  ( f)  Name  of  journal  FollowecJ  by  no  punctua- 
tion, unclc*rsc orc*cl,  and  alilirc*vi.ilc*d  acccirding  to  Index  Mc'dicus.  (4) 
Year  of  publication;  |.5|  Volume  number:  Do  not  include*  issue  number 
or  month  e*xc  e*pl  in  the*  c ase*  of  a su|ijile*me*nl  or  when  jiaginaticin  is 
nol  c onse*c  ulivc*  ifiroughoul  tfie  volume*.  |6|  Inclusive  page  numbers. 
Do  nol  omil  digits. 

Ex.implc*:  Itor.i  1 1,  l).iiiiic*m  1 1,  St.inforcl  W,  c*t  .il:  A guiclc*line  fcir  lilocicl 

use*  during  surgc*ry.  Am  I (Jin  I^Jlhol  1979;71:680-692. 

HOOKS 

1 1 1 Author(s):  Use*  the*  surname*  follciwc*d  fiy  initials  without  jiunctua- 
lion.  Ihc*  n.mic*s  of  .ill  .uithors  should  lie*  given  unle*ss  the*re  are  more 
Ih.in  lhrc*e*,  in  wliic  h c .ise*  the*  name's  of  the*  first  three  authors  are  used 
fcillowc'cl  by  "c*l  .il."  12 1 Title,  Cajiitalize  the  first  and  last  word  and 
c'.ic  h word  ih.il  is  nol  an  .irlic  le,  |ire*(icisiticin,  or  conjunction  of  less 
Ih.m  four  lc*llc*rs.  | f|  Edition  number,  |41  Editor's  name.  |5]  Place  of 
publication,  (hi  Publisher,  (71  Year,  (H]  Inclusive  page  numbers.  Do 
not  omit  digits. 

Ex.impk‘:  l)c*(iolc*  (I  , Spann  E,  I lursi  KA  |r,  c*l  al;  Hodsido  Examina- 

tion in  ( ardinvasc  iilar  M('di(  ino,  c*cl  2,  Smith  |T  (c*d).  New 
York,  McC.r.iw  Hill  Co,  1986,  pj)  2J-J7. 

ILLUSTRATIONS  should  fic*  submiltc'd  in  duplicate  in  an  envelope* 
(p.ijic'r  c lijis  should  nol  lie*  use*cl  on  illustrations  since  the  indentation 
lhe*y  make*  may  show  on  re'produc  ticin).  Legends  should  fie  typc'd, 
cloublc*-spac  c*d  on  .i  sc'par.ilc*  shcH'l  of  |ia|ier.  Pholograjihic  material 
should  be*  high-c  onirast  glossy  jirints.  Patients  must  be  unreccignizafile 
in  phc)lcigra|ihs  unless  spe*c  ific  wrille*n  conse'nt  has  bc*e*n  ofitainc'd,  in 
whic  h c .ise*  .i  c eijiy  of  the*  authori/alion  should  ac  c cimjiany  the 
m.inusc  rijit.  Omit  illtiJraliotts  witich  do  not  increase  understanding 
ol  text.  Illusir.ilions  must  fie*  limite*cl  lo  a reasonalile  number  (four  il- 
luslr.ilions  should  be*  .idc'ciu.ilc*  for  a manuscrijil  of  4 to  5 tyjie'd  pages). 
Ihc*  following  inlormalion  should  fie  ty|ie*cl  on  a lalic'l  and  affixc'd  to 
the*  li.u  k of  e*ac  h illusir.ilion:  figure  numbc*r,  title  of  manusc  rijit,  name 
of  se'iiior  .uilhor,  .ind  arrow  indicating  top. 

TABLES  should  be*  se'lf-ex|ilanatory  and  should  sujiplement,  not 
duplicate*,  the*  le*xl.  E.u  h should  be*  tyjic’d  on  a sejiarate*  shee't  of  pajier, 
numbe*rc'cl,  .md  have*  a brie'f  de*sc  rijitive  title. 

ACKNOWLEDGMENTS  are*  Ihe*  author's  jirerogative;  howewer, 
ac  knowle'dgmeni  ol  lec  hnic  i.ins  and  other  remuneratc'd  jiersonnel  for 
c .irrying  oul  routine'  c)|ier.ilicins,  or  of  resident  physicians  who  merely 
c .ire*  for  |i.ilic*nls  .is  jiarl  of  ihc'ir  hosjiital  clutie's  is  discouragc'd.  More 
,ic  c c'pl.ible*  .K  kiiowlc'clgme'iils  inc  lude  those  of  intellectual  or  profes- 
sional jiartic  i|i.iticin. 

GALLEY  PROOES  will  be*  maile'd  to  the  jirincitial  author  for  corre’c- 
lioiis.  kepriiil  ordc'rs  forms  will  accompany  galle*y  jiroofs. 


NEW  MEMBERS 


Applications  for  membership  have  been  re- 
ceived from  the  following  physicians  by  the 
respective  parish  medical  societies  as  of  De- 
cember 8, 1987.  The  Louisiana  State  Medical 
Society  is  pleased  to  welcome: 

■ East  Baton  Rouge 

William  A.  Anderson  III,  MD 

5412  Dijon  Dr,  Baton  Rouge  70808 

1982,  LSU  School  of  Medicine,  New  Orleans 
internal  medicine 

Gerald  M.  Barber,  MD 

4609  North  Blvd,  Baton  Rouge  70806 
1984,  LSU  School  of  Medicine,  New  Orleans 
family  practice 

Jeffrey  G.  Breaux,  MD 

6300  Main  St,  Bldg  G,  Suite  A,  Zachary  70791 

1983,  Tulane  University  School  of  Medicine 
obstetrics  & gynecology 

N.  Joseph  Deumite,  MD 

5228  Dijon  Dr,  Baton  Rouge  70809 
1980,  LSU  School  of  Medicine,  New  Orleans 
internal  medicine 

George  W.  Evans,  MD 
3600  Florida  Blvd,  Baton  Rouge  70806 
1954,  University  of  Pennsylvania  School  of 
Medicine 
pathology 

Robert  S.  Fields,  MD 

4950  Essen  Lane,  Baton  Rouge  70809 
1975,  Jefferson  Medical  College,  Philadel- 
phia 

radiation  oncology 

Milton  G.  Fort,  MD 

5825  Airline,  Baton  Rouge  70805 
1977,  Baylor  College  of  Medicine 
obstetrics  & gynecology 

Nancy  N.  Grinton,  MD 
8212  Summa  Ave,  Suite  B,  Baton  Rouge 
70809 

1979,  LSU  School  of  Medicine,  New  Orleans 
anesthesiology 

Richard  D.  Hanson,  MD 

5422  Dijon,  Baton  Rouge  70808 

1982,  LSU  School  of  Medicine,  New  Orleans 

diagnostic  radiology 


Roberta  J.  Hawk,  MD 

1401  North  Foster  Dr,  Baton  Rouge  70806 

1982,  Tulane  University  School  of  Medicine 
dermatology 

Francis  H.  Henderson,  MD 
673  East  Airport  Ave,  Baton  Rouge  70806 
1962,  Howard  University  School  of  Medi- 
cine, Washington,  DC 
obstetrics  & gynecology 

Daniel  H.  McNeill  Jr,  MD 

2041  Silverside,  Suite  A,  Baton  Rouge  70808 

1973,  University  of  North  Carolina  School 
of  Medicine 

diagnostic  radiology 

Beverly  W.  Ogden,  MD 

1516  Jefferson  Hwy,  New  Orleans  70121 

1983,  Tulane  University  School  of  Medicine 
pathology 

Glen  J.  Schwartzberg,  MD 
7525  Picardy  Ave,  Suite  C,  Baton  Rouge 
70809 

1980,  Tulane  University  School  of  Medicine 
vascular  surgery 

Mark  C.  Shoptaugh,  MD 

8212  Summa  Ave,  Suite  B,  Baton  Rouge 
70809 

1984,  LSU  School  of  Medicine,  New  Orleans 
anesthesiology 

Sterling  E.  Sightler,  MD 

7662  Goodwood  Blvd,  Suite  B201,  Baton 
Rouge  70806 

1982,  LSU  School  of  Medicine,  New  Orleans 
obstetrics  & gynecology 

■ Iberia 

L.  Barrow  Bourgeois,  MD 
1409  Church  St,  Jeanerette  70544 

1974,  LSU  School  of  Medicine,  Shreveport 
family  practice 

■ Jefferson 

Grace  A.  Banuchi,  MD 
151  Meadowcrest  St,  Suite  C,  Gretna  70056 
1976,  University  of  Puerto  Rico  School  of 
Medicine 
pediatrics 


Mark  Dal  Corso,  MD 
3456  Jurgeus,  Metairie  70002 
1984,  University  de  Monterrey  Instituto 
Ciencias  de  la  Salud  Facultad  Medicina, 
Mexico 
pediatrics 

Thiem  Dang,  MD 

105-C  Westbank  Expressway,  Gretna  70053 

1972,  Faculte  Mixte  de  Medecine  et  de  Phar- 
macie  University  de  Saigon,  South  Viet- 
nam 

family  practice 

Edmund  K.  Kerut,  MD 

4500  Wichers  Dr,  Marrero  70072 
1982,  University  of  Mississippi  School  of 
Medicine 
cardiology 

John  J.  Knox,  MD 

PO  Box  949,  Civic  Dr,  Port  Sulphur  70083 

1973,  University  of  Iowa  College  of  Medi- 
cine 

internal  medicine 

Elenita  S.  Mata,  MD 

151  Meadowcrest  St,  Gretna  70056 

1980,  Institute  of  Medicine  Far  Eastern  Uni- 
versity, Philippines 

pediatrics 

Joseph  H.  Puente,  MD 

4315  Houma  Blvd,  Metairie  70002 

1981,  American  University  of  the  Caribbean 
internal  medicine 

Richard  R.  Roniger,  MD 

4315  Houma  Blvd,  Metairie  70002 

1968,  LSU  School  of  Medicine,  New  Orleans 

psychiatry 

■ Lafayette 

Jack  A.  Hurst,  MD 

110  Hospital  Dr,  Lafayette  70503 

1979,  LSU  School  of  Medicine,  New  Orleans 

neurological  surgery 

Steven  Jacobs,  MD 

4212  West  Congress,  Lafayette  70503 

1982,  University  of  California  School  of 
Medicine,  Los  Angeles 

ophthalmology  ^ 

JOURNAL  VOL  140  FEBRUARY  3 


Earl  Washington  Jr,  MD 

850  North  Pierce  St,  Lafayette  70501 

1978,  Tulane  University  School  of  Medicine 
gastroenterology 

M Rapides 

Vernon  W.  Cantwell,  MD 

PO  Box  669,  Olla  71465 
1986,  University  of  Texas  Medical  School, 
San  Antonio 
general  practice 

Dave  M.  Rayburn,  MD 

390  Griffith  St,  Pineville  71360 

1982,  LSU  School  of  Medicine,  Shreveport 
general  surgery 

■ River  Parishes 

Vern  E.  Meyer,  MD 

16A  Storehouse  Lane,  Destrehan  70047 
1974,  Medical  College  of  Virginia  Common- 
wealth University  School  of  Medicine 
pediatrics 

■ Shreveport 

Motaz  Albahra,  MD 

1850  Martin  Dr  #922,  Bossier  City  71111 

1979,  Faculty  of  Medicine  University  of 
Aleppo,  Syria 

pathology 

Bruce  A.  Baethge,  MD 

PO  Box  33932,  Dept  of  Internal  Medicine, 
Shreveport  71130 

1978,  University  of  Texas  Southwestern 
Medical  School 

internal  medicine 

Michael  J.  Cone,  MD 

8701  Creswell  Rd,  Shreveport  71104 

1979,  LSU  School  of  Medicine,  Shreveport 
neonatal/ perinatal 

Roan  L.  Flenniken,  MD 

8730  Youree  Dr,  Shreveport  71115 

1983,  LSU  School  of  Medicine,  Shreveport 
internal  medicine 

Patrick  T.  Gallagher,  MD 

2510  Bert  Kouns  Industrial  Loop,  Shreve- 
port 71129 

1982,  LSU  School  of  Medicine,  Shreveport 
emergency  medicine 

B.  Kishore  Gupta,  MD 

PO  Box  33932,  Dept  of  Psychiatry,  Shreve- 
port 71130 

1974,  Kasturba  Medical  College,  Mysore 
University,  India 
psychiatry 


William  H.  Haynie  Jr,  MD 

1035  Creswell,  Shreveport  71101 

1982,  LSU  School  of  Medicine,  Shreveport 
internal  medicine 

Mark  E.  Janulewicz,  MD 

1035  Creswell,  Shreveport  71101 
1975,  University  of  Nebraska  College  of 
Medicine 
family  practice 

Jacque  T.  LaBarre,  MD 

207  Winged  Foot,  Shreveport  71106 

1983,  LSU  School  of  Medicine,  Shreveport 
obstetrics  & gynecology 

Judy  D.  Laviolette,  MD 

2532  Bert  Kouns,  Suite  E107,  Shreveport 
71118 

1984,  LSU  School  of  Medicine,  Shreveport 
internal  medicine 

Susan  A.  Lee,  MD 

2355  Bert  Kouns,  Suite  E107,  Shreveport 
71118 

1984,  University  of  Texas  Medical  School, 
San  Antonio 
family  practice 

Larry  C.  Moore,  MD 

1035  Creswell,  Shreveport  71101 

1980,  University  of  Texas  Medical  Branch, 
Galveston 

cardiology 

John  M.  Provenza,  MD 

2533  Bert  Kouns,  Suite  107,  Shreveport  71118 
1984,  LSU  School  of  Medicine,  Shreveport 
internal  medicine 

Hiram  M.  Vazquez,  MD 

1530  Line  Ave,  Shreveport  71104 

1981,  Universidad  Nordestana,  Dominican 
Republic 

anesthesiology 

■ St.  Tammany 

Thomas  J.  Dewey  III,  MD 

1045  Elorida  Ave,  Slidell  70458 

1967,  LSU  School  of  Medicine,  New  Orleans 

orthopedic  surgery 

Joseph  A.  Pedone,  MD 

1323  South  Tyler,  Covington  70458 
1977,  LSU  School  of  Medicine,  New  Orleans 
internal  medicine 

■ Tangipahoa 

Brian  C.  Ball,  MD 

1003  Delural  Blvd,  Hammond  70403 
1984,  LSU  School  of  Medicine,  New  Orleans 
anesthesiology 


■ Terrebonne 

Conchita  J.  Lazarraga,  MD 
1978  Industrial  Blvd,  Houma  70363 

1977,  University  of  the  East,  Philippines 
pediatrics 

Ronald  J.  Long,  MD 

1978  Industrial  Blvd,  Houma  70363 

1978,  Indiana  University  School  of  Medicine 
obstetrics  & gynecology 

Ursula  S.  Long,  MD 

1978  Industrial  Blvd,  Houma  70363 

1978,  Northwestern  University  Medical 
School 

anesthesiology 

■ Intern/ Resident  Members 

CALCASIEU 

Francine  A.  Manuel,  MD 

1000  Walters,  Lake  Charles  70601 

1985,  LSU  School  of  Medicine,  New  Orleans  , 

family  practice  i 

■ Service  Members 

SHREVEPORT 

Daniel  J.  Culkin,  MD 

PO  Box  33932,  Dept  of  Urology,  Shreveport 
71130 

1979,  Creighton  University  School  of  Med- 
icine, Omaha 

urology 


I 

I 


4 JOURNAL  VOL  140  FEBRUARY 


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JOURNAL  VOL  140  FEBRUARY  5 


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A ml*  Uir 

V5s\-.4.ViJ* 


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Dista  Products  Company 

Diviston  of  Eli  Lilly  and  Company 
Indianapolis,  Indiana  46285 
Mfd  by  Eli  Lilly  industries,  Inc 
Carolina,  Puerto  Rico  00630 


□ ISTA 


Computer-generated  molecu 
structure  of  cephalexin 
hydrochloride  monohydrate 


® 1987,  DISTA  PRODUCTS  COMPANY  KX-9008-B-849336 


Convenient  500-mg  b.i.d. 
dosage  and  demonstrated 
effectiveness  for 
treatment  of: 

□ skin  and  skin  structure  infections^^ 

□ uncomplicated  cystitis^ 

□ pharyngitis* 


• New  hydrochloride  salt  form  of  cephalexin— 
requires  no  conversion  in  the  stomach  before 
absorption 

• Well-tolerated  therapy 

• May  be  taken  without  regard  to  meals 

^or  other  indicated  infections,  250-mg  tablets  available 
brq.i.d.  dosage 


=*riced  less  than  Keflexlcephaiexin) 


Keftab  is  contraindicated  in  patients  with  known  allergy  to  the 
cephalosporins  and  should  be  given  cautiously  to  penicillin- 
sensitive  patients. 

Penicillin  is  the  drug  of  choice  in  the  treatment  and  prevention 
of  streptococcal  infections,  including  the  prophylaxis 
of  rheumatic  fever. 


K 'Due  to  susceptible  strains  of  Staphylococcus.aureus  and/or  /3-hemolytic  streptococci. 

Due  to  susceptible  strains  of  Escherichia  coli.  Proteus  mira'bilis.  and  Klebsiella  sp. 

If  Due  to  susceptible  strains  of  group  A 0-hemolytic  streptococci. 


KEFTAB" 

(cephalexin  hydrochloride  monohydrate) 

Summary:  Consult  the  package  literature  for 
prescribing  information. 

Indications  and  Usage: 

Respiratory  tract  infections  caused  by  susceptible 
strains  of  Streptococcus  pneumoniae  and  group  A 
i3-hemolytic  streptococci. 

Skin  and  skin  structure  infections  caused  by  sus- 
ceptible strains  of  Staphylococcus  aureus  and/or 
/3-hemolytic  streptococci. 

Bone  infections  caused  by  susceptible  strains  of 
S aureus  and/or  Proteus  mirabilis. 

Genitourinary  tract  infections,  including  acute  pros- 
tatitis, caused  by  susceptible  strains  of  Escherichia 
coli,  P mirabilis,  and  Klebsiella  sp. 

Contraindication:  Known  allergy  to  cephalosporins. 

Warnings:  KEFTAB  SHOULD  BE  ADMINISTERED 
CAUTIOUSLY  TO  PENICILLIN-SENSITIVE  PA- 
TIENTS. PENICILLINS  AND  CEPHALOSPORINS 
SHOW  PARTIAL  CROSS-ALLERGENICITY.  POSSI- 
BLE REACTIONS  INCLUDE  ANAPHYLAXIS. 
Administer  cautiously  to  allergic  patients. 
Pseudomembranous  colitis  has  been  reported  with 
virtually  all  broad-spectrum  antibiotics.  It  must  be 
considered  in  differential  diagnosis  of  antibiotic- 
associated  diarrhea.  Colon  flora  is  altered  by  broad- 
spectrum  antibiotic  treatment,  possibly  resulting  in 
antibiotic-associated  colitis. 

Precautions: 

• Discontinue  Keftab  in  the  event  of  allergic  reac- 
tions to  it. 

• Prolonged  use  may  result  in  overgrowth  of  nonsus- 
ceptible  organisms. 

• Positive  direct  Coombs’  tests  have  been  reported 
during  treatment  with  cephalosporins. 

• Keftab  should  be  administered  cautiously  in  the 
presence  of  markedly  impaired  renal  function.  Al- 
though dosage  adjustments  in  moderate  to  severe 
renal  impairment  are  usually  not  required,  careful 
clinical  observation  and  laboratory  studies  should 
be  made. 

• Broad-spectrum  antibiotics  should  be  prescribed 
with  caution  in  individuals  with  a history  of  gas- 
trointestinal disease,  particularly  colitis. 

• Safety  and  effectiveness  have  not  been  determined 
in  pregnancy  and  lactation.  Cephalexin  is  excreted 
in  mother’s  milk.  Exercise  caution  in  prescribing 
Keftab  for  these  patients. 

• Safety  and  effectiveness  in  children  have  not  been 
established. 

Adverse  Reactions: 

• Gastrointestinal,  including  diarrhea  and,  rarely,  nau- 
sea and  vomiting.  Transient  hepatitis  and  chole- 
static Jaundice  have  been  reported  rarely. 

• Hypersensitivity  in  the  form  of  rash,  urticaria,  angio- 
edema,  and,  rarely,  erythema  multiforme,  Stevens- 
Johnson  syndrome,  or  toxic  epidermal  necrolysis. 

• Anaphylaxis  has  been  reported. 

• Other  reactions  have  included  genital/anal  pruri- 
tus, genital  moniliasis,  vaginitis/vaginal  discharge, 
dizziness,  fatigue,  headache,  eosinophilia,  neutro- 
penia, and  thrombocytopenia:  reversible  interstitial 
nephritis  has  been  reported  rarely. 

•Cephalosporins  have  been  implicated  in  trigger- 
ing seizures,  particularly  in  patients  with  renal 
impairment. 

• Abnormalities  in  laboratory  test  results  included 
slight  elevations  in  aspartate  aminotransferase 
(AST,  SCOT)  and  alanine  aminotransferase  (ALT, 
SGPT).  False-positive  reactions  for  glucose  in  the 
urine  may  occur  with  Benedict’s  or  Fehling's  solu- 
tion and  Clinitest®  tablets  but  not  with  Tes-Tape® 
(Glucose  Enzymatic  Test  Strip,  USR  Lilly). 

PV  2060  DPP  [091887]  849336 


BLOOD  PRESSURE  CONTROL 

IN  CHILDREN 


The  following  is  reprinted  by  permission  at  the  request  of  the  Louisiana 
State  Medical  Society  Committee  on  Chronic  Diseases.  It  is  excerpted 
from  the  National  Heart,  Lung,  and  Blood  Institute's  "Report  of  the 
Second  Task  Force  on  Blood  Pressure  Control  in  Children  - 1987"  which 
appeared  in  Pediatrics  [1987;79(1);1-25], 

All  physicians  who  care  for  children  3 years  of  age  through  adolescence  should  be 
encouraged  to  measure  blood  pressures  (BPs)  once  a year,  when  the  child  is  well.  This 
is  because  BP  is  a physiologic  parameter,  which  when  elevated  becomes  a risk  factor, 
either  for  the  development  of  hypertension  itself  or  for  the  development  of  premature 
cardiovascular  morbidity,  if  not  during  childhood,  then  during  adulthood.  BP  measure- 
ment should  be  included  in  the  physical  examination  as  part  of  the  continuing  care 
of  the  child,  not  as  an  isolated  procedure.  BPs  should  also  be  measured  in  symptomatic 
children,  children  in  emergency  rooms  and  intensive  care  units,  and  in  high-risk  in- 
fants, because  an  elevated  BP  may  complicate  certain  diseases  or  be  a marker  of  future 
hypertension.  At  the  time  of  examination,  the  patient  or  parent  should  be  told  that  the 
BP  is  normal,  high  normal,  or  hypertensive  and  whether  further  surveillance  is  indicated. 
It  should  be  clearly  stated  that  the  finding  of  single  modestly  elevated  reading  does 
not  constitute  a diagnosis  of  hypertension  but  does  indicate  the  need  for  further  evalua- 
tion including  repeated  measurements  over  time.  Children  with  severely  elevated 
readings  should  be  evaluated  immediately. 


8 JOURNAL  VOL  140  FEBRUARY 


Norton  W.  Voorhies,  MD,  Editor 


ECG  OF  THE  MONTH 


ELEGANT,  BUT  INCOMPLETE 

JORGE  I.  MARTINEZ-LOPEZ,  MD 


The  tracing  shown  below  consists  of  seven  leads  from  a 12-lead  scalar  ECG  received  at  the  Heart 
Station  without  patient  identification  or  information  relative  to  the  clinical  diagnosis  and  treat- 
ment. 


What  is  your  diagnosis?  Elucidation  is  on  page  13. 


JOURNAL  VOL  140  FEBRUARY  11 


REPORTING  AIDS  CASES  IN  LOUISIANA 


WHO  SHOULD  REPORT? 

Every  physician  is  required  by  law  to  report  any  case  or  suspected  case  of  AIDS  which  he  or  she  is  attending, 
has  examined,  or  has  prescribed  for  (Louisiana  Sanitary  Code,  Chapter  II,  §2:004). 

WHAT  SHOULD  BE  REPORTED? 

The  presence  of  a reliably  diagnosed  disease  at  least  moderately  indicative  of  an  underlying  cellular  immune 
deficiency,  with  no  other  known  underlying  cause  of  cellular  immune  deficiency  nor  any  other  cause  of  reduced 
resistance  reported  to  be  associated  with  that  disease.  This  involves  completion  of  a two-page  case  report 
form  (available  from  the  Epidemiology  Section  or  any  parish  health  unit)  to  determine  if  the  person  meets 
the  Centers  for  Disease  Control  AIDS  surveillance  case  definition. 

WHEN  SHOULD  1 REPORT? 

The  report  should  be  made  promptly  at  the  time  the  physician  first  visits,  examines  or  prescribes  for  the 
patient  (Louisiana  Sanitary  Code,  Chapter  II,  §2:004). 

WHERE  SHOULD  1 REPORT? 

A diagnosed  or  suspected  case  of  AIDS  should  be  reported  directly  to  the  Epidemiology  Section  in  New 
Orleans. 

By  phone:  (504)  568-5005 

By  mail:  La.  Office  of  Preventative  and  Public  Health  Services 
Epidemiology  Section 
PO  Box  60630 
Room  615 

New  Orleans,  LA  70160 

WHY  REPORT  AIDS  CASES? 

In  addition  to  being  required  by  law,  monitoring  the  distribution  and  characteristics  of  patients  with  AIDS 
is  the  only  method  currently  available  for  detecting  changes  in  the  epidemiology  of  Human  Immunodefi- 
ciency Virus  (HIV).  Knowledge  of  the  impact  of  HIV  on  Louisiana  residents  can  help  detect  new  or  unusual 
modes  of  transmission  and  assist  in  targeting  high  risk  groups  for  education  and  prevention  programs. 

CONFIDENTIALITY  CONCERNS 

All  reports  are  kept  absolutely  confidential.  Names  of  patients,  physicians  or  hospitals  are  not  released  under 
any  circumstances. 

ECG  of  the  Month 

Case  presentation  is  on  page  11. 

DIAGNOSIS  — Atrial  fibrillation  with  advanced  AV  block 

Because  of  the  total  lack  of  information  with  respect 
to  the  patient  whose  tracing  is  shown  here,  the  dis- 
cussion to  follow  starts  with  a description  of  the  ECG 

(findings  and  ends  with  comments  on  their  possible 
clinical  significance. 

DISCUSSION 

The  tracing  raises  a number  of  important  questions, 
f none  of  which  can  be  answered  at  this  time:  What  is 
the  cardiac  diagnosis?  What  symptoms  and  clinical 
findings  are  present?  What  did  previous  ECGs  show? 
What  medications  is  the  patient  receiving?  What  are 
the  values  for  serum  levels  of  potassium,  magnesium, 
and  of  antiarrhythmic  drugs? 

The  basic  cardiac  rhythm  is  atrial  fibrillation.  The 
tracing  does  not  display  P waves  — of  either  sinus  or 
ectopic  origin  — nor  atrial  flutter  waves.  Instead,  atrial 
i activity  is  represented  by  the  constantly  irregular,  low- 
! amplitude  waviness  of  the  isoelectric  baseline. 

Examination  of  the  tracing  for  ventricular  elec- 
trical activity  reveals  two  important  findings.  First, 

I QRS  complexes  are  narrow.  This  is  consistent  with 
normal  intraventricular  conduction  of  atrial  fibrilla- 
tory  impulses  that  succeed  in  penetrating  the  distal 
conducting  system  of  the  heart.  Second,  the  lengthy 
R-R  intervals,  equivalent  to  ventricular  rates  of  about 
28  to  30  a minute,  are  a manifestation  of  significant 
AV  block.  Although  QRS  complexes,  at  first  glance, 
appear  to  recur  regularly,  measurement  of  the  R-R 
intervals  with  a set  of  calipers  clearly  shows  that  they 
! are  not  of  equal  length,  but  rather  vary  slightly.  This 
I finding  confirms  that  the  AV  block  is  advanced  and 
not  complete. 

Most  important,  perhaps,  are  three  other  ECG 
abnormalities:  prominent  U waves,  prolongation  of 
I the  QT  interval  (0.52  sec),  and  prolongation  of  the 
QU  interval  (0.68  sec). 

Prominent  positive  U waves  are  best  seen  in  pre- 
; cordial  leads  V2  and  V4;  U waves  are  inverted  in 
precordial  lead  V6.  Because  the  amplitude  of  the  nor- 
mal U wave  is  5%  to  25%  of  the  amplitude  of  the 
preceding  T wave,  the  U wave  is  termed  "prominent" 


when  it  is  equal  to  or  taller  than  the  amplitude  of  the 
T wave  in  the  same  lead,  especially  in  leads  V2  through 
V4.  The  polarity  of  the  normal  U wave  is  usually  con- 
cordant with  the  normal  T wave.  Negative  U waves 
are  nearly  always  abnormal  and  their  clinical  signif- 
icance is  determined  by  the  clinical  situation  in  which 
they  are  found. 

There  is  no  doubt  that  the  QT  interval  is  pro- 
longed, but  the  superimposition  of  the  prominent  U 
wave  in  the  downstroke  of  the  T wave  clearly  extends 
total  repolarization  of  the  ventricles  further.  QT  and 
QU  intervals  prolongation  have  been  correlated  with 
an  increased  susceptibility  to  sudden  cardiac  death 
provoked  by  malignant  ventricular  arrhythmias. 
Therefore,  it  is  important  to  identify  and  correct  pos- 
sible predisposing  and  etiologic  factors. 

When  all  the  ECG  findings  listed  above  are  taken 
into  consideration,  two  major  factors  are  likely  re- 
sponsible: a combination  of  multiple  electrolyte  de- 
ficiencies and  the  concomitant  use  of  antiarrhythmic 
drug  therapy.  The  combination  of  QT  and  QU  pro- 
longation with  prominent  U waves  is  most  often  en- 
countered when  the  electrolyte  deficiency  involves 
potassium  and  magnesium.  Intracellular  deficiency  of 
either  or  both  ions  may  not  be  accurately  reflected  in 
serum  levels  until  total  body  stores  are  markedly  re- 
duced. Therefore,  depletion  of  both  potassium  and 
magnesium  can  exist  even  when  serum  levels  are  nor- 
mal. 

Hypokalemia  and  hypomagnesemia,  alone  or  in 
concert,  can  exert  arrhythmogenic  effects  on  the  heart. 
These  electrolyte  abnormalities  can  also  modify  the 
pharmacologic  effects  of  antiarrhythmic  drugs  on  the 
heart.  For  example,  deficiency  of  either  or  both  elec- 
trolytes predisposes  to  digitalis  toxicity  by  narrowing 
the  therapeutic  range  of  digitalis;  in  other  words,  the 
amount  of  digitalis  required  to  produce  toxic  effects 
is  significantly  reduced.  This  is  especially  true  when 
these  electrolyte  deficits  are  found  in  patients  with 
advanced  cardiac  disease  taking  digitalis.  Other  an- 
tiarrhythmic drugs  that  may  be  partly  responsible  for 
the  abnormal  findings  on  the  ECG  shown  here  in- 
clude the  Class  I agents:  quinidine,  procainamide, 
and  disopyramide. 

The  "elegant  record"  has  been  defined  as  one 


JOURNAL  VOL  140  FEBRUARY  13 


Specify  Adjvinctive 


which  ''provides  a message,  both  subtle  and  yet  com- 
manding." When  using  an  elegant  record  as  a teach- 
ing tool,  four  steps  have  been  suggested:  pure  de- 
scription, statement  of  the  obvious,  detection  of 
unusual  or  unexpected  events,  and  discussion  of  "ex- 
periments that  could  be  performed  to  support  (or  de- 
stroy) the  explanation  offered."  In  my  presentation, 
this  prescribed  approach  is  used.  Unfortunately,  the 
lack  of  information  makes  this  tracing  elegant,  but 
incomplete.  ■ 

SELECTED  REFERENCES 

1.  Burch  GE,  Giles  TD:  The  importance  of  magnesium  deficiency  in  cardi- 
ovascular disease.  Am  Heart  } 1977;94:649-657. 

2.  Hishida  H,  Cole  JS,  Surawicz  B:  Negative  U wave:  A highly  specific  but 
poorly  understood  sign  of  heart  disease.  Am  / Cardiol  1982;49:2030-2036. 

3.  Geddes  LA:  The  elegant  record.  Physiologist  1982;25:448-449. 

4.  Commerford  PJ,  Lloyd  EA:  Arrhythmias  in  patients  with  drug  toxicity, 
electrolyte,  and  endocrine  disturbances.  Med  Clin  North  Am  1984;68:1051- 
1078. 

5.  Surawicz  B,  Knoebel  S,  Long  QT:  Good,  bad  or  indifferent.  / Am  Coll 
Cardiol  1984;4:398-413. 

6.  Stewart  DE,  Ikram  H,  Espiner  EA,  et  al:  Arrhythmogenic  potential  of 
diuretic-induced  hypokalemia  in  patients  with  mild  hypertension  and 
ischemic  heart  disease.  Br  Heart  J 1985;54:290-297. 


Dr.  Martinez-Lopez  is  a specialist  in  cardiovascular  diseases  affiliated 
with  the  Cardiology  Service,  Department  of  Medicine  at  William 
Beaumont  Army  Medical  Center  in  El  Paso,  TX. 

The  opinions  and  assertions  contained  herein  are  the  private  views  of  the 
author  and  not  to  be  construed  as  official  or  as  reflecting  the  views  of 
the  Department  of  the  Army  or  Department  of  Defense. 


14  JOURNAL  VOL  140  FEBRUARY 


Each  capsule  contains  5 mg  chlordiazepoxide  HCl  and  2.5  mg 
clidinium  bromide 


Please  consult  complete  prescribing  information,  a summary  of  which 
follows: 


* 


Indications:  Based  on  a review  of  this  drug  by  the  National  Acad- 
emy of  Sciences— National  Research  Council  and/or  other  informa- 
tion, FDA  has  classified  the  indications  as  follows: 

“Possibly”  effective:  as  adjunctive  therapy  in  the  treatment  of  peptic 
ulcer  and  in  the  treatment  of  the  irritable  bowel  syndrome  (irritaole 
colon,  spastic  colon,  mucous  colitis)  and  acute  enterocolitis. 

Final  classification  of  the  less-than-effective  indications  requires  fur- 
ther investigation. 


Contraindications:  Glaucoma;  prostatic  hypertrophy,  benim  bladder 
neck  obstruction;  hypersensitivity  to  chlordiazepoxide  HCl  and/or 
clidinium  Br. 

Warnings:  Caution  patients  about  possible  combined  effects  with  alco- 
hol and  other  CNS  aepressants,  and  against  hazardous  occupations 
requiring  complete  mental  alertness  {e.g.,  operating  machinery,  driving). 
Physical  and  psychological  dependence  rardy  reported  on  recommended 
doses,  but  use  caution  in  administering  Librium®  (chlordiazepoxide  HCl/ 
Roche)  to  known  addiction-prone  individuals  or  those  who  might 
increase  dosage;  withdrawal  symptoms  (including  convulsions)  reported 
following  discontinuation  of  the  drug. 

Usage  in  Pregnancy:  Use  of  minor  tranouilizers  during  first 
trimester  should  ahnost  always  be  avoided  because  of  increased 
risk  of  congeniul  malformations  as  suggested  in  several  studies. 
Consider  possibility  of  premancy  when  instituting  therapy. 

Advise  patients  to  mscuss  therapy  if  they  intend  to  or  do 
become  pregnant. 

As  with  all  anticholinergics,  inhibition  of  lactation  may  occur. 

Precautions:  In  elderly  and  debilitated,  limit  dosage  to  smallest  effective 
amount  to  preclude  ataxia,  oversedation,  confusion  (no  more  than 
2 capsules/day  initially;  increase  gradually  as  needed  and  tolerated). 
Though  generally  not  recommended,  if  combination  therapy  with  other 
psychotropics  seems  indicated,  carefully  consider  pharmacology  of 
agents,  particularly  potentiating  drugs  such  as  MAO  inhibitors,  pheno- 
thiazines.  Observe  usual  precautions  in  presence  of  impaired  renal  or 
hepatic  function.  Paradoxical  reactions  reported  in  psychiatric  patients. 
Employ  usual  precautions  in  treating  anxiety  states  with  evidence  of 
impending  depression;  suicidal  tendencies  may  be  present  and  protective 
measures  necessary.  Variable  effects  on  blood  coagulation  reported  very 
rarely  in  patients  receiving  the  drug  and  oral  anticoagulants;  causal  rela- 
tionship not  established. 

Adverse  Reactions:  No  side  effects  or  manifestations  not  seen  with 
either  compound  alone  reported  with  Librax.  When  chlordiazepoxide  HCl 
is  used  alone,  drowsiness,  ataxia,  confusion  may  occur,  especially 
in  elderly  and  debilitated;  avoidable  in  most  cases  by  proper  dosage 
adjustment,  but  also  occasionally  observed  at  lower  dosage  ranges.  Syn- 
cope reported  in  a few  instances.  Also  encountered:  isolated  instances  of 
skin  eruptions,  edema,  minor  menstrual  irregularities,  nausea  and  con- 
stipation, extrapyramidal  symptoms,  increased  and  decreased  libido — 
all  infrequent,  generally  controlled  with  dosage  reduction;  changes  in 
EEG  patterns  may  appear  during  and  after  treatment;  blood  dyscrasias 
(including  agranulocytosis),  jaundice,  hepatic  dysfunction  reported 
occasionally  with  chlordiazepoxide  HCl,  making  periodic  blood  counts 
and  liver  function  tests  advisable  during  protracted  therapy.  Adverse 
effects  reported  with  Librax  typical  of  anticholinergic  agents,  i.e.,  dry- 
ness of  mouth,  blurring  of  vision,  urinary  hesitancy,  constipation.  Con- 
stipation has  occurred  most  often  when  Librax  therapy  is  combined 
with  other  spasmolytics  and/or  low  residue  diets. 


Roche  Products  Inc. 
Manati,  Puerto  Rico  00701 


P.l  0186 


flistiiiie 

for  the  Peacemaker. 

In  irritable  bowel  S5mdrome*  anxiety  can  aggravate  intestinal  symptoms,  which  may 
further  intensify  anxiety  — a distressing  cycle  of  brain/bowel  conflict.  Librax  intervenes  with 
two  well-known  compoimds.  The  Librium®  (chlordiazepoxide  HCl/Roche)  component 
safely  relieves  anxiety.  And  Quarzan®  (chdinium  bromide/Roche)  provides  antisecretory 
and  antispasmodic  action  to  relieve  discomfort  associated  with  intestinal  hypermotility. 

Dual  action — for  peace  between  brain  and  bowel.  Because  of  possible  CNS  effects,  caution 
patients  about  engaging  in  activities  requiring  complete  mental  alertness.  Specify  Adjimctive 

LIBRi!\X 

Each  capsule  contains  5 mg  chlordiazepoxide  HCl 
and  2.5  mg  chdinium  bromide 


*Librax  has  been  evaluated  as  possibly  effective  as  adjunctive  therapy  in  the  treatment  of  peptic  ulcer  and  the  irritable  bowel  syndrome. 
Copyright  ( 1987  by  Roche  Products  Inc.  All  rights  reserved.  Please  see  summary  of  prescribing  information  on  adjacent  page. 


OTOLARYNGOLOGY/ 

HEAD  & NECK  SURGERY  REPORT 


( 

I 

1 

! 

I 

J 

J 


EVALUATION  AND  MANAGEMENT 
OF  NASOPHARYNGEAL  CARCINOMA 


D.L  BREEN,  MD;  PAUL  A.  BLAIR,  MD,  FACS 


Nasopharyngeal  carcinoma  is  a challenge  to  the 
physician  because  of  its  location  and  capacity  for 
misdiagnosis.  A case  report  illustrating  the  ability 
of  this  cancer  to  mask  itself  behind  neurologic, 
otologic,  and  nasal  symptoms  is  presented. 
Evaluation  requires  a careful  head  and  neck  exam, 
nasopharyngeal  biopsy,  and  computed  tomography 
scan.  Radiation  therapy  remains  the  standard 
treatment  of  these  lesions  as  well  as  of  their  neck 
metastases.  Epstein-Barr  virus  antibodies  can  be 
sensitive  indicators  in  the  diagnosis  and 
management  of  nasopharyngeal  carcinoma. 


Nasopharyngeal  carcinoma  (NPC)  is  the  most 
frequently  misdiagnosed  head  and  neck  malig- 
nancy. Although  representing  less  than  2%  of  head 
and  neck  malignancies,  cancers  of  the  nasopharynx  j 
carry  a dismal  prognosis.  This  is  related  to  the  pro- 
pensity of  the  tumor  to  spread  into  the  abundant  lym- 
phatic drainage  of  the  nasopharynx.  Also,  the  tumor 
causes  few  symptoms  when  small  so,  when  diag- 
nosed, most  tumors  are  already  large. ^ , 

The  majority  of  nasopharyngeal  cancers  are  ep-  j 
idermoid  in  derivation  with  lymphomas,  adenocar- 
cinomas, melanomas,  and  sarcomas  comprising  less 
than  15%.  The  three  main  types  of  epidermoid  car- 
cinomas are  keratinizing,  nonkeratinizing,  and  un-  ] 
differentiated.  Lymphoepithelioma  is  a term  used  to 
describe  nonkeratinizing  and  undifferentiated  carci- 
nomas if  abundant  lymphocytes  are  found  on  histo- 
logical sampling. 2 Lymphoepitheliomas  are  associ- 
ated with  a better  prognosis  and  higher  survival  rates. ^ 

CASE  REPORT 

A 56-year-old  white  male  came  to  the  Otolaryngology 
clinic  with  complaints  of  right  facial  pain,  headaches 
radiating  to  base  of  the  head,  and  nasal  obstruction. 


16  journal  VOL  140  FEBRUARY 


Past  medical  history  revealed  that  the  patient  had  had 
pneumatic  equalization  tubes  placed  in  both  ears  two 
years  ago  for  bilateral  serous  otitis  media  and  had  had 
a septoplasty  six  months  ago  for  nasal  obstruction. 
No  nasopharyngeal  biopsy  was  performed  nor  was 
an  unusual  nasopharyngeal  examination  recorded.  On 
physical  examination,  the  patient  had  a large  mass 
obstructing  the  right  choana  and  a right  posterior  neck 
node  measuring  2 cm  in  diameter.  The  mass  extended 
into  the  nasopharyngeal  walls  on  either  side  of  the 
choana  but  was  confined  to  the  nasopharynx.  Com- 
puted tomography  (CT)  scan  showed  no  bony  in- 
volvement or  erosion  into  the  base  of  the  skull  and 
no  intracranial  extension.  Biopsy  of  the  lesion  through 
the  nose  confirmed  poorly  differentiated  squamous 
cell  carcinoma.  Epstein-Barr  virus  (EBV)  titer  for  an- 
tibodies to  the  viral  capsid  antigen  (VCA)  was  1:640, 
which  is  seropositive.  The  patient  had  a complete 
course  of  radiation  for  treatment  of  the  primary  site 
and  the  extension  of  the  neck.  Presently  he  has  no 
evidence  of  disease. 

EPIDEMIOLOGY 

There  are  several  risk  factors  related  to  the  develop- 
ment of  nasopharyngeal  carcinoma.  The  two  most 
significant  epidemiological  characteristics  of  this  dis- 
ease are  race  and  exposure  to  the  EBV.  Southern 
Chinese  have  a risk  118  times  average  of  developing 
this  cancer  whereas  for  North  American-born  Chinese 
the  risk  is  still  seven  times  average.  EBV  tests  are  not 
only  important  diagnostic  aids  but  also  are  useful  in 
following  the  patient  for  evidence  of  recurrence.^  EBV 
DNA  is  found  in  aU  three  types  of  NPC.^ 

Exposure  to  smoke,  chemical  fumes,  and  diet  of 
salted  fish  have  been  linked  with  NPC.  Recently  the 
role  of  cigarette  smoking  as  an  etiological  factor  was 
found  to  be  consistent  with  a casual  relationship.^ 

DISCUSSION 

The  most  common  presenting  symptom  is  a lump  in 
the  neck;  followed  by  nasal  obstruction,  epistaxis,  and 
various  otologic  complaints  (Table  1).^-^  The  triad  of 
hearing  loss,  maxillary  neuralgia,  and  palatal  hemi- 
paresis  is  almost  pathognomonic  of  a nasopharyngeal 
neoplasm. 

Diagnosis  of  NPC  requires  a thorough  head  and 
neck  examination,  including  visual  examination  of  the 


TABLE  1 

MOST  COMMON  PRESENTING  SYMPTOMS  OF 
NASOPHARYNGEAL  CARCINOMA 

1. 

Cervical  lymph  node  enlargement 

30-70% 

2. 

Nasal  symptoms 

epistaxis 

9% 

obstruction 

25% 

3. 

Otologic  symptoms 
hearing  loss 
infection 
earache 
tinnitus 
dizziness 

20-40% 

4. 

Cranial  Nerve  Dysfunction 

8-25% 

nasopharynx  by  mirror  or  endoscope,  and  an  evalu- 
ation of  cranial  nerve  function.  Nasopharyngeal  bi- 
opsy can  usually  be  done  transnasally  in  the  office  or 
clinic  with  use  of  topical  anesthesia.  CT  scan  of  the 
complete  extent  of  the  lesion  is  important  to  deter- 
mine bony  or  intracranial  extension.  Lymphatic  drain- 
age from  the  nasopharynx  is  directly  into  lateral  re- 
tropharyngeal nodes  with  connection  to  nodes  around 
the  jugular  foramen  and  to  cranial  nerves  IX  through 
XII.  Neck  drainage  commonly  leads  to  enlargement 
of  the  jugulodigastric  and  posterior  cervical  nodes  in 
the  spinal  accessory  chain.  An  enlarged  posterior  neck 
node  should  alert  the  physician  to  perform  a thorough 
search  of  the  nasopharynx,  the  most  common  site  of 
origin  of  the  primary  leading  to  posterior  triangle  node 
involvement. 

Distant  metastasis  is  most  frequently  to  bone, 
then  to  lung,  liver,  and  distant  lymph  nodes.  Al- 
though chest  roentgenograms  and  liver  profile  are 
routinely  obtained,  bone  scans  are  reserved  for  those 
patients  presenting  with  bone  symptoms  or  elevated 
serum  calcium  levels. 

Treatment  of  NPC  consists  of  from  5000  to  7500 
rads  to  the  primary  and  the  neck  as  weU  as  intracav- 
itary boosts  with  radium  seed  implants.^  Referral  for 
radiation  therapy  should  be  preceded  by  a careful 
dental  evaluation  and  treatment  as  needed.  Surgery 
is  not  recommended  due  to  the  location  of  the  tumor 
at  the  base  of  the  skull  in  the  nasopharynx  — a major 
obstacle  to  resection. 

Staging  has  been  shown  to  be  a major  indicator 
in  prognosis,  with  extension  beyond  the  nasopharynx 

JOURNAL  VOL  140  FEBRUARY  17 


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REMEMBER  TO  WRITE  “DO  NOT  SUBSTITUTE.  ” 
IT  PROTECTS  YOUR  DECISION. 


Copyright  © 1987  by  Roche  Products  Inc.  All  rights  reserved. 


The  cut  out  "V"  design  is  a registered  trademark  of  Roche  Products  Inc. 


TABLE  2 

STAGING  OF  NASOPHARYNGEAL  CARCINOMA 
ACCORDING  TO  TNM  SYSTEM 


T,  one  site  in  nasopharynx  involved 

Tz  two  sites  in  nasopharynx  involved  (generally  the  posterior- 
superior  or  lateral  walls) 

T3  extension  into  the  nasal  cavity  or  outside  the  nasopharynx 

T4  invasion  of  bone  and/or  cranial  nerve  involvement 

No  no  palpable  node 

Ni  single  lymph  node  less  than  3 cm 

Na  a)  single  node  3-6  cm 

b)  multiple  homolateral  nodes,  each  less  than  or  equal  to  6 
cm 

N3  a)  homolateral  node  greater  than  6 cm 

b)  bilateral  nodes 

c)  contralateral  nodes 


and  involvement  of  neck  nodes  highly  negative  prog- 
nosticators. The  primary  tumor/regional  nodes/dis- 
tant metastasis  classification  is  presented  in  Table  2. 
Five-year  survival  rates  range  from  80%  to  90%  for 
Stage  I,  60%  to  70%  for  Stage  11,  40%  to  50%  for  Stage 
III,  and  10%  to  40%  for  Stage  IV. ^ Recent  studies  with 
adjuvant  chemotherapy  show  promising  responses  in 
Stage  III  and  IV  disease.® 

Recurrences  in  the  nasopharynx  are  treated  with 
either  surgery  or  radiation  boost,  whereas  neck  re- 
currences are  best  treated  with  radical  neck  dissec- 
tion. 

EPSTEIN-BARR  VIRUS  TITERS 

The  seropositive  rates  in  NPC  patients  for  EBV  as- 
sociated antibodies  — early  antigen  (EA)  and  VGA  — 
range  from  42%  to  100%.^  Of  this  group,  anti-VGA 
IgA  and  anti-EA  IgG  are  the  most  sensitive  indicators 
in  the  diagnosis  and  management  of  patients  with 
NPG.i" 

A total  of  85%  of  patients  with  nonkeratinizing 
and  undifferentiated  carcinoma  types  have  antibody 
responses  versus  a 16%  response  in  controls.^  In  con- 
trast, only  35%  of  keratinizing  squamous  cell  patients 
had  positive  responses.  This  makes  anti-VGA  IgA  and 
anti-EA  IgG  important  diagnostic  tools  for  following 
NPG  patients  with  the  two  most  serious  types  of  na- 
sophryngeal  carcinoma.  As  the  patient  enters  remis- 
sion, response  rates  fall  to  18%,  while  response  rates 
with  recurrence  or  distant  metastases,  increase  to  85% 
to  100%. 


Serial  anti- VGA  and  anti-EA  titers  after  radiation 
therapy  can  alert  the  physician  to  occult  recurrence 
or  metastases.  Gontinued  high  viral  titers  after  radio- 
therapy can  be  interpreted  as  indicating  the  presence 
of  residual  disease. 

SUMMARY 

NPG  is  a formidable  opponent  to  the  head  and  neck 
cancer  surgeon  mainly  because  of  its  late  presentation 
and  propensity  for  misdiagnosis.  A good  head  and 
neck  exam,  nasopharyngeal  biopsy,  and  GT  scan  of 
the  nasopharynx  complete  the  diagnostic  work-up. 
The  mainstay  of  treatment  is  radiation  therapy  with 
excellent  cure  rates  if  started  early.  The  use  of  EBV 
antibody  titers  is  a sensitive  method  for  detecting  oc- 
cult disease.  ■ 

REFERENCES 

1.  Neel  HB  III:  A Prospective  Evaluation  of  Patients  With  Nasopharyngeal 
Carcinoma:  An  Overview.  / Otolaryngol  1986;15:137-144. 

2.  Fox  R and  Graham  WP.  Carcinoma  of  the  Nasopharynx  and  Posterior 
Pharyngeal  Wall.  Surg  Clin  North  Am  1986;66:97-108. 

3.  Rahima  M et  al.  Carcinoma  of  the  Nasopharynx:  An  Analysis  of  91  Cases 
and  a Comparison  of  Differing  Treatment  Approaches.  Cancer  1986;58:843- 
849. 

4.  Neel  HB  et  al.  Application  of  Epstein-Barr  Virus  Serology  to  the  Diag- 
nosis and  Staging  of  North  American  Nasopharyngeal  Carcinoma.  Oto- 
laryngol Head  Neck  Surg  1983;91:255-262. 

5.  Raab-Traub  N et  al.  The  Differentiated  Form  of  Nasopharyngeal  Carci- 
noma Contains  Epstein-Barr  Virus.  DNA.  Int  J Cancer  1987;39:25-29. 

6.  Mabuchi  K,  Bross  DS  and  Kessler  II.  Cigarette  Smoking  and  Nasopha- 
ryngeal Carcinoma.  Cancer  1985;55:2874-2876. 

7.  Schabinger  P et  al.  Carcinoma  of  the  Nasopharynx:  Survival  and  Patterns 
of  Recurrence.  Int  J Radiat  Oncol  Biol  Phys  1985;11:2081-2084. 

8.  Chatani  M et  al.  Radiation  Therapy  for  Nasopharyngeal  Carcinoma. 
Retrospective  Review  of  105  Patients  Based  on  a Survey  of  Kansai  Cancer 
Therapist  Group.  Cancer  1986;57:2267-2271. 

9.  Lynn  T-C  et  al.  Epstein-Barr  Virus  — Associated  Antibodies  and  Serum 
Biochemistry  in  Nasopharyngeal  Carcinoma.  Laryngoscope  1984;94:1485- 
1488. 

10.  Neel  HB  III,  Pearson  GR,  and  Taylor  WF.  Antibodies  to  Epstein-Barr 
Virus  in  Patients  With  Nasopharyngeal  Carcinoma  and  in  Comparison 
Groups.  Ann  Otol  Rhinol  Laryngol  1984;93:477-481. 


Drs.  Breen  and  Blair  are  from  the  Dept  of  Otolaryngology-Head  and 
Neck  Surgery  at  Tulane  University  School  of  Medicine  in  New  Orleans. 

Reprint  requests  should  be  sent  to  Paul  A.  Blair,  MD,  Department  of 
Otolaryngology-Head  and  Neck  Surgery,  1430  Tulane  Ave, 

New  Orleans,  LA  70112. 


JOURNAL  VOL  140  FEBRUARY  21 


CAT  FMDAR 


March 


March  6-11 

9th  Annual  Mammoth  Mountain  Emergency  Medicine, 

Mammoth  Lakes,  California.  Contact:  Medical  Conferences,  Inc, 
CME  Travel  Service,  1615  S Mission  Road,  Suite  3,  Fallbrook,  CA 
92028;  (714)650-4156. 

March  7-9 

World  Congress  III  on  Cancers  of  the  Skin,  The  Lincoln 
Hotel  Post  Oak,  Houston.  Contact:  University  of  Texas  M.D. 
Anderson  Hospital  and  Tumor  Institute,  Office  of  Conference  Ser- 
vices HMB  131,  1515  Holcombe  Blvd,  Houston,  TX  77030; 
(713)792-2222. 


1988  Annual  Meeting 
Louisiana  State  Medical  Society 
March  10-13,  Lake  Charles 


March  12-27 

Australia/New  Zealand  - Diagnostic  Imaging  Down  Under, 

Australia  and  New  Zealand.  Contact:  Medical  Seminars  Inter- 
national, 21915  Roscoe  Blvd,  Suite  222,  Canoga  Park,  CA  91304; 
(818)719-7380. 

March  14-18 

2nd  Annual  Update  on  Primary  Care,  Steamboat  Springs, 
Colorado.  Contact:  Larry  G.  McLain,  MD,  Dept  of  Pediatrics, 
Loyola  University  Medical  Center,  2160  South  First  Ave, 
Maywood,  Illinois  60153;  (312)531-3195. 

March  16-19 

Highlights  in  Women's  Health  Care,  Orlando,  Florida.  Con- 
tact: Susan  Larson,  Director,  Scott  and  White  Office  of  Continu- 
ing Medical  Education,  2401  South  31st  St,  Temple,  TX  76508; 
(817)774-4083. 

March  17-18 

Assessment  of  Clinical  Competence  in  Specialty  Medicine, 

Toronto  Hilton  Harbour  Castle  Hotel,  Toronto.  Contact: 
American  Board  of  Medical  Specialties,  One  Rotary  Center  #805, 
Evanston,  IL  60201. 

March  17-19 

Advanced  Concepts  in  Rigid  Skeletal  Fixation,  Delta  Moun- 


tain Inn,  Whistler,  British  Columbia.  Dr.  M.  Kaburda,  Suite 
208,  600  Royal  Ave,  New  Westminster,  BC;  (604)524-1301. 

March  17-20 

Hair  Replacement  Surgery,  Los  Angeles.  (Zontact:  American 
Academy  of  Facial  Plastic  and  Reconstructive  Surgery,  1101  Ver- 
mont Ave  NW,  Suite  404,  Washington,  DC  20005. 

March  19-27 

A Study  Tour  in  England  on  Public  and  Private  Care  In- 
novations for  the  Aged,  London,  Oxford,  and  Canterbury. 
Contact:  Pat  Ashton,  Holbrook  Travel,  3540  NW  13th  Street, 
Gainesville,  FL  32609;  (800)451-7111. 

March  25-26 

Advances  in  Emergency  Medicine:  Toxicology  and  Infec- 
tious Disease,  Mission  Bay,  California.  Contact:  Continuing 
Education  in  Health  Sciences,  UCLA  Extension,  PO  Box  24901, 
Los  Angeles,  CA  90024;  (213)825-7257. 

March  25-27 

Rigid  Fixation  of  the  Facial  Skeleton,  Walt  Disney  World 
Village,  Lake  Buena  Vista,  Florida.  Contact:  Mary  Appleton, 
Dept  of  Oral  and  Maxillofacial  Surgery,  Northwestern  University 
Dental  School,  (312)908-5243. 

March  26  - April  12 

Orthopedic  Emergencies,  Waiohai  & Poipu  Beach  Hotels, 
Kauai,  Hawaii.  Contact:  Edith  S.  Bookstein,  Conference  Manage- 
ment Associates,  PO  Box  2586,  La  Jolla,  CA  92038;  (619)454-3212. 

March  28-30 

NIH  Consensus  Development  Conference/Kidney  Stones: 
Prevention  and  Treatment,  Bethesda,  Maryland.  Contact: 
Conference  Registrar,  Prospect  Associates,  Suite  500,  1801  Rockville 
Pike,  Rockville,  MD  20852;  (301)468-MEET. 


April 


April  8-10 

Louisiana  Psychiatric  Association/Mississippi  Psychiatric 
Association  Joint  Meeting,  Natchez,  Mississippi.  Charlene 
Smith,  Louisiana  Psyciatric  Association,  PO  Box  15765,  New 
Orleans,  LA  70175;  (504)891-1030. 

April  13-17 

4th  Annual  Family  Medicine  Review,  Austin,  Texas,  Dept 
of  Continuing  Medical  Education,  Scott  & White,  2401  South  31st 
St,  Temple,  TX  76508;  (817)774-2350. 


22  JOURNAL  VOL  140  FEBRUARY 


April  20-24 

2nd  Annual  Review  Course  in  Critical  Care  Medicine, 

Washington,  DC.  Contact:  Svetlana  Lisanti,  Program  Coor- 
dinator, Center  for  Bio-Medical  Corhmunication,  (201)385-1808. 

April  22-24 

3rd  International  Interdisciplinary  Conference  on  Hyperten- 
sion in  Blacks,  Baltimore.  Contact:  Cecile  Cate,  Conference  Coor- 
dinator, International  Society  on  Hypertension  in  Blacks,  69  Butler 
St  SE,  Atlanta,  GA  30303;  (404)589-3810. 

April  23-24 

The  Cutting  Edge  1988/Innovations  in  Psychotherapy:  Help- 
ing Individuals  and  Couples  to  Change,  Hotel  Del  Cor- 
onado, Sna  Diego.  Contact:  Office  of  Continuing  Medical  Educa- 
tion, UC  San  Diego  School  of  Medicine,  La  Jolla,  CA  92093; 
(619)534-3940. 


May 


May  2-4 

NIH  Consensus  Development  Conference:  Cochlear  Im- 
plants, Bethesda,  Maryland.  Contact:  Conference  Registrar,  Pro- 
spect Associates,  Suite  500,  1801  Rockville  Pike,  Rockville,  MD 
20852;  (30D468-MEET. 

May  4-6 

6th  Regions  II  & III  High  Blood  Pressure  Conference/New 
Challenges  — Creative  Solutions,  Richmond,  Virginia.  Paula 
A.  Ciaverella  or  Joann  T.  Richardson,  Virginia  Dept  of  Health, 
Division  of  Chronic  Disease  Control,  109  Governor  St,  Madison 
Bldg,  Richmond,  VA  23219;  (804)786-4065. 

May  5-7 

The  National  Conference  on  Health  Care  Leadership  and 
Management,  Sheraton  Harbor  Island,  San  Diego.  Contact: 
Sherry  Mason,  American  Academy  of  Medical  Directors,  4830  W 
Kennedy  Blvd,  Suite  648,  Tampa,  EL  33609-2517;  (813)287-2000. 

May  13  - June  3 

Cruise/ Seminar  on  Risk  Management  and  Comparative 
Medicolegal  Issues,  Hong  Kong,  China,  and  Japan.  Inter- 
national Conferences,  Suite  C,  189  Lodge  Ave,  Huntington  Sta- 
tion, NY  11746;  (800)521-0076,  (516)549-0869. 


June 


June  1-4 

9th  Conference  on  Computer  Applications  in  Radiology, 

HUton  Head  Island,  South  Carolina.  Contact:  Ms.  Janice  Ford, 
Continuing  Education  Coordinator,  Dept  of  Radiology  Hospital  of 
the  University  of  Pennsylvania,  3400  Spruce  St,  Philadelphia,  PA 
19104;  (215)662-6904,  (215)662-6982. 

June  16-18 

33rd  Annual  Great  Smokey  Mountain  Pediatric  Seminar, 

Park  Vista  Hotel,  Gatlinburg,  Tennessee.  Contact:  Dr.  San- 
dra Loucks,  University  of  Tennessee  Medical  Center,  Dept  of 
Pediatrics,  1924  Alcoa  Hwy,  Knoxville,  TX  37920;  (615)544-9331. 


JOURNAL  VOL  140  FEBRUARY  23 


MICROSURGERY  1987: 

THE  LSU  EXPERIENCE 


JAMES  W.  WADE,  MD;  ROY  F.  BRABHAM,  MD; 
L.  FRANKLYN  ELLIOTT,  MD 


24  JOURNAL  VOL  140  FEBRUARY 


Microsurgery  was  introduced  into  the  Louisiana 
State  Lfniversity  program  of  Plastic  and 
Reconstructive  Surgery  in  1978.  Since  1983,  78  free 
tissue  transfers  have  been  performed  in  75  patients 
at  LSU-associated  teaching  hospitals  with  a success 
rate  of  92% . Much  has  been  accomplished  in  the 
realm  of  refinement  of  microsurgical  techniques 
such  that  morbidity  of  both  donor  site  and 
recipient  site  is  minimized.  This  paper  attempts  to 
outline  indications  for  and  selection  of  free  tissue 

transfer. 


WITH  AN  EVER-INCREASING  demand  for  safe  and 
effective  means  of  providing  coverage  to  trau- 
matic and  surgical  defects,  free  tissue  transfer  has 
become  a viable  approach  toward  management  of  such 
problems.^  Since  the  introduction  of  microsurgery  into 
the  LSU  program  of  Plastic  and  Reconstructive  Sur- 
gery in  the  late  70s,  considerable  success  has  been 
achieved  in  terms  of  both  immediate  and  late  recon- 
struction of  difficult  wounds  and  anatomic  defects  by 
utilizing  free  tissue  transfer.  Over  the  past  four  years, 
we  have  specifically  addressed  our  efforts  and  atten- 
tions toward  refinement  of  standard  microsurgical 
techniques  to  provide  not  only  effective  bony/soft  tis- 
sue reconstruction  but  also  optimal  functional  and 
cosmetic  results. 

Our  microsurgical  experience  as  a whole  has  dealt 
largely  with  two  parameters,  namely  free  tissue  trans- 
fer and  replantation.  The  objective  of  this  paper,  how- 
ever, is  to  outline  the  indications  and  selection  of 
specific  flaps  available  for  free  tissue  transfer.  This 
entity  itself  offers  significant  versatility  in  selection  of 
the  transferred  tissue  to  accommodate  a specific  de- 
fect with  optimal  results  in  terms  of  both  function  and 
cosmetic  appearance  of  donor  and  recipient  sites  (Ta- 
ble 1).  Since  July  1983,  we  have  performed  78  free 
tissue  transfers  at  the  LSU-associated  teaching  hos- 
pitals. We  have  had  six  failures  for  a success  rate  of 
[ 92%,  exceeding  the  internationally  accepted  85%  to 

I 90%  successful  transfer  figures.^  Three  of  the  failed 
transfers  were  in  host-compromised  patients  and  may 
possibly  represent  errors  in  patient  selection.  Post- 
I operative  complications,  aside  from  flap  failure,  have 
required  re-operation  in  eight  instances  in  the  im- 
mediate post-operative  period.  Other  complications 


TABLE  1 

FREE  TISSUE  TRANSFER  — 

AVAILABLE  TISSUES  | 

Skin 

Muscle-skin 

Fascia 

Bone 

Skin-fascia 

Omentum 

Muscle 

Jejunum 

TABLE  2 

FREE  TISSUE  TRANSFER  - 

- 78  FLAPS 

No. 

Failed 

Success 
Rate  (%) 

Latissimus  Dorsi 

26 

3 

84 

Forearm  Fasciocutaneous 

9 

0 

100 

Scapular  Fasciocutaneous 

7 

0 

100 

Gracilis 

3 

0 

100 

Jejunum 

8 

1 

87.5 

Omentum 

2 

0 

100 

Rectus  Abdominis 

14 

1 

92 

Tensor  Fascia  Lata 

1 

0 

100 

Fibula 

3 

0 

100 

Iliac  Crest 

2 

1 

50 

Temporalis  Fascia 

1 

0 

100 

Toe  to  Hand 

1 

0 

100 

Thoracic  Fascia 

1 

0 

100 

78 

6 

92% 

have  been  limited  to  seroma  formation  at  donor  sites 
and  superficial  infections. 

There  is  a vast  array  of  flaps  available  for  free 
tissue  transfer  and  the  variety  of  flaps  utilized  in  this 
series  demonstrates  the  versatility  and  refinements  of 
the  science  of  free  tissue  transfer  over  the  last  few 
years  (Table  2).  Objectives  of  transfer  are  first  to  pro- 
vide coverage  of  a specific  defect  followed  by  resto- 
ration of  function  and  cosmetic  appearance.  Desired 
thickness,  presence  or  absence  of  skin  and/or  bone, 
size  of  defect,  anatomic  location  of  recipient  site,  and 
future  requirements  (eg,  weight-bearing,  sensibility, 
delayed  bone  grafts)  are  all  taken  into  account  in  se- 
lecting an  appropriate  donor  tissue  for  free  transfer. 
Additional  considerations,  by  no  means  of  little  im- 
portance, are  donor  site  morbidity  and  cosmetic  ap- 
pearance. In  the  early  days  of  free  tissue  transfer  these 
latter  considerations  were  of  less  significance  than 
they  are  today. 


JOURNAL  VOL  140  FEBRUARY  25 


Fig  1.  Open  tibia  fracture  with  exposed  bone,  ten- 
don, vessels  and  deficient  soft  tissue  cov- 
erage. 


Recipient  sites  for  transfer  have  been  primarily 
in  the  lower  extremity  where  defects  in  the  distal  third 
of  the  leg  have  in  the  past  been  relegated  to  ampu- 
tation in  many  instances  (Table  3,  Figs  1,  2).  Especially 
amenable  to  free  tissue  transfer  is  exposed  bone  with 
chronic  osteomyelitis,  a condition  for  which  both  clin- 
ical and  laboratory  evidence  exists  validating  trans- 
ferred revascularized  muscle  (coupled  with  adequate 
debridement)  provides  for  expeditious  and  effective 
healing  (Figs  3, 4),^'  ^ In  the  absence  of  infected  tissues, 
an  appropriate  alternative  to  free  muscle  transfer  is 
revascularized  fascia  or  fasciocutaneous  flaps  which 
provide  a durable  yet  thin  cover  to  soft  tissue  defects. 
Transfers  to  the  lower  extremity  have  included  those 

26  JOURNAL  VOL  140  FEBRUARY 


Fig  2.  Follow-up  of  rectus  abdominis  free  flap  with 
skin  graft  after  14  months. 


to  weight-bearing  areas  of  the  foot  and  these  have 
withstood  the  daily  trauma  of  ambulation.  Some  can 
be  innervated  at  the  time  of  transfer  to  allow  for  return 
of  protective  and  tactile  sensibility. 

We  have  not,  however,  limited  our  experience  to 
the  lower  extremity  and  we  have  utilized  free  tissue 
transfer  for  defects  to  the  upper  extremity  as  well  as 
the  head  and  neck.  These  areas  are  often  found  to  be 


TABLES 

FREE  TISSUE  TRANSFER  — 

RECIPIENT  SITES 

Number 

Head  & Neck 

15 

Upper  Extremity 

11 

Lower  Extremity 

52 

78 

Fig  3.  Chronic  osteomyelitis  following  open  tibia 
fracture. 


Fig  4.  Follow-up  of  latissimus  dorsi  free  flap  with 
skin  graft  after  six  months. 


in  need  of  reconstruction  in  response  to  both  trau- 
matic and  surgical  defects.  One  area  of  particular  im- 
portance is  the  cervical  esophagus  where  ablative  sur- 
gery has  previously  resulted  in  a considerable 
functional  and  cosmetic  defect  requiring  cervical 
esophagostomy  and  gastrostomy  for  feeding  and  se- 


Fig  5.  Pre-operative  barium  esophagogram  dem- 
onstrating subtotal  cervical  esophageal  oc- 
clusion secondary  to  recurrent  laryngeal 
carcinoma. 

cretion  management  — results  adversely  affecting 
quality  of  life  in  these  unfortunate  patients.  With 
transfer  of  a segment  of  jejunum  to  restore  continuity 
to  the  alimentary  canal,  patients  are  able  to  eat  and 
handle  their  own  secretions  without  difficulty,  and 
thereby  an  improvement  in  the  quality  of  life  is 
achieved  (Figs  5-7).^'  ^ Cutaneous  defects  of  the  face 
and  hand  require  thin,  pliable  tissues  with  an  ac- 
ceptable cosmetic  appearance.  Free  transfers  common 
to  these  areas  are  usually  derived  from  the  skin/fascia 
of  the  forearm  or  the  fascia  alone  from  either  the  arm, 
back,  or  temple  coupled  with  a skin  graft. 

Operative  procedures  of  this  magnitude  are  not 
without  complication,  but  fortunately  most  can  be 
effectively  managed  without  loss  of  the  transferred 
tissue  or  an  increase  in  hospital  stay.  With  added 
experience,  operative  time  averages  four  and  one-half 
hours.  The  patient  is  maintained  in  an  intensive  care 
setting  48  to  72  hours  post-operatively  and  the  ex- 
pected date  of  discharge  is  12  to  14  days  following 
free  tissue  transfer.  We  feel  that  this  relatively  short 
post-reconstruction  hospital  stay  significantly  de- 
creases the  overall  cost  of  hospitalization  in  patients 
with  difficult  reconstructive  problems. 

SUMMARY 

It  is  our  feeling  that  microsurgery  in  the  realm  of  free  ► 
JOURNAL  VOL  140  FEBRUARY  27 


Fig  6.  Segment  of  jejunum  as  free  transfer  in  place 
in  neck  foliowing  surgicai  resection  of  re- 
current carcinoma  (tracheostome  is  at  bot- 
tom). 


Fig  7.  One  month  post-operative  follow-up  esoph- 
agogram  demonstrating  patency  and  mu- 
cosai  folds  of  jejunum  in  neck. 


28  JOURNAL  VOL  140  FEBRUARY 


tissue  transfer  has  much  to  offer  to  the  surgical  com- 
munity and  is  relevant  to  all  specialties  within  it.  With 
greater  experience  and  attention  to  detail,  refinements 
have  been  and  will  continue  to  be  made  in  efforts  to 
provide  optimal  patient  care  and  management.  ■ 

REFERENCES 

1.  Daniel  RK,  Taylor  GI:  Distant  transfer  of  an  island  flap  by  microvascular 
anastomoses.  Plast  Reconstr  Surg  1973;52:111-117. 

2.  Shaw  WW:  Microvascular  free  flaps:  The  first  decade.  Clin  Plast  Surg 
1983;10:3-20. 

3.  Mathes  SJ,  Alpert  BS,  Chang  N:  Use  of  the  muscle  flap  in  chronic  osteo- 
myelitis: Experimental  and  clinical  correlation.  Plast  Reconstr  Surg 
1982;69:815-828. 

4.  Ger  R:  Muscle  transposition  for  the  treatment  and  prevention  of  chronic 
post-traumatic  osteomyelitis  of  the  tibia.  / Bone  Joint  Surg  1977;59A:784- 
791. 

5.  Jurkiewicz  MJ:  Vascularized  intestinal  graft  for  reconstruction  of  the  cer- 
vical esophagus  and  pharynx.  Plast  Reconstr  Surg  1965;36:509-517. 

6.  McConnel  MS,  Hester  JR,  Nahai  F,  et  al:  Free  jujenal  grafts  for  recon- 
struction of  pharynx  and  cervical  esophagus.  Arch  Otolaryngol  Head  Neck 
Surg  1981;107:476-481. 


Dr.  Wade  received  his  medical  degree  from  LSU  School  of  Medicine  in 
New  Orleans  in  1978  and  completed  a general  surgery  residency  at  the 
Medical  College  of  Georgia  and  plastic  surgery  training  at  LSU.  He  is 
currently  a plastic  and  reconstructive  surgeon  in  private  practice  in 
Baton  Rouge  and  holds  a clinical  appointment  within  the  Dept  of 
Surgery,  Division  of  Plastic  Surgery  at  LSU  Medical  Center.  He  is  also 
affiliated  with  Our  Lady  of  the  Lake  Regional  Medical  Center  in 

Baton  Rouge. 

Dr.  Brabham  is  a graduate  of  the  LSU  School  of  Medicine  in  Shreveport 
and  completed  general  surgery  and  plastic  surgery  training  at  the 
University  of  Wisconsin.  He  is  presently  in  private  practice 
in  Baton  Rouge  and  is  affiliated  with  Our  Lady  of  the 
Lxike  Regional  Medical  Center. 

Dr.  Elliott  completed  his  medical  education  at  Vanderbilt  and  his 
general  surgery  residency  with  Tulane.  He  followed  with  plastic  surgery 
training  at  Emory  University  and  held  a clinical  appointment  with  the 
LSUMC  Department  of  Plastic  Surgery.  He  has  recently  moved  to 
Atlanta  where  he  is  in  private  practice. 

Reprints  will  not  be  available. 


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JOURNAL  VOL  140  FEBRUARY  29 


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Physicians  Recognition  Award 

Eighteen  physicians  from  the  state  of  Louisiana  were  awarded  the  Physicians  Recognition  Award  [PRA]  during 
November,  1 987.  This  award  is  presented  by  the  American  Medical  Association  to  physicians  who  have  voluntarily 
completed  1 50  hours  of  continuing  medical  education  during  a consecutive  three-year  time  period.  Of  these  1 50 
hours,  at  least  60  must  be  in  AMA/PRA  Category  1 . These  eighteen  individuals  and  the  cities  in  which  they  reside 
are  presented  below. 

Alexandria 

John  Allen  Baldridge,  MD* 

Keith  Alan  Holmes,  MD* 

Baton  Rouge 

Chester  C.  Coles,  Jr.,  MD 
Ngo  Khai,  MD 
Gilbert  B.  Meyers,  MD 
Reza  Sheybani,  MD* 

Buras 

Philippe  Logaglio,  MD* 


Covington 

William  James  Mitchell,  MD 

Kenner 

Michael  John  Jennings,  MD 

Metairie 

Leon  Lapleau  Mclntire,  MD* 

New  Iberia 

Edward  W.  Dauterive,  MD 


New  Orleans 

Kenneth  Allen  Bell,  MD 
Robert  Charles  Fortenberry,  MD 
John  A.  Kalmar,  MD 
Larry  Edward  Millikan,  MD 
Ernest  O.  Svenson,  MD 

Shreveport 

David  Thomas  Henry,  MD 
Jack  Selwyn  Resneck,  MD 


* These  individuals  are  members  of  the  Louisiana  State  Medical  Society 


30  JOURNAL  VOL  140  FEBRUARY 


SONOGRAPHIC  EVALUATION  OF 
ACUTE  BACTERIAL  MENINGITIS 


KRISHNA  GRAVOIS,  MD 


Acute  bacterial  meningitis  may  result  in  compli- 
cations despite  appropriate  treatment.  Cribside, 
portable,  real-time  ultrasound  can  be  easily  per- 
formed without  transporting  a sick  infant  who  may 
be  on  a mechanical  ventilator  and  other  life  support- 
ing devices.  The  examination  is  safe  and  low- 
cost  as  compared  to  computed  tomography  (CT), 
and  requires  no  sedation.  Intracranial  changes  can  be 
easily  and  repeatedly  demonstrated.  Sonographic 
findings  vary  from  normal  (Figs  1,  2)  to  evidence  of 
echogenic  sulci,  ventriculomegaly,  extra-axial  fluid 
collection  (EAF),^'^  diffuse  or  localized  intense  paren- 
chymal echos,  ventriculitis,^'  ^ gyral  infarction,^  and 
brain  abscess.^'  ^ 

MATERIALS  AND  METHODS 

Between  1984  and  1987,  approximately  60  proven  cases 
of  acute  bacterial  meningitis  were  treated  at  our  hos- 
pital. Complicated  cases  were  evaluated  mostly  by 
cranial  CT,  but  recently  we  have  been  using  portable 
real-time  ultrasound  (7.5  MHz  transducer)  and  ob- 
taining sagittal  and  coronal  scans  at  cribside  without 
the  need  to  transport  to  a sick  baby. 


CASE  REPORT 

An  infant  of  38  weeks  gestation,  weighing  7 lbs  4 oz 
was  born  without  complication.  During  that  stay,  the 
baby  had  several  spells  of  apnea  for  which  cranial 
ultrasound  yielded  results  normal  for  a neonate  (Figs 
1,  2).  The  baby  was  discharged  on  the  seventh  day 
in  good  condition. 

Approximately  two  months  after  discharge,  the 
baby  was  readmitted  for  upper  respiratory  infection, 
vomiting,  diarrhea,  and  dehydration.  Symptomatic 
treatment  was  initiated,  but  on  the  next  day  the  baby 
developed  a stiff  neck  and  constant  crying.  Blood  cul- 
ture grew  Hemophilus  influenzae  type  b.  Spinal  punc- 
ture was  performed  with  cerebrospinal  fluid  findings 
of  a RBC  count  of  500/ (jlL,  a WBC  count  of  575/ |xL  with 
83%  neutrophils  and  17%  lymphocytes,  a glucose  level 
of  1 mg/dL,  and  a protein  level  of  >380  mg/dL.  Gram 
stain  showed  many  bacteria. 

Besides  the  bacterial  meningitis  due  to  septi- 
cemia, the  baby  developed  acute  renal  failure,  acute 
respiratory  failure,  and  pericarditis.  Chest  x-ray  dem- 
onstrated cardiomegaly.  An  echocardiogram  revealed  ► 

JOURNAL  VOL  140  FEBRUARY  31 


ACKNOWLEDGMENTS 


My  thanks  to  Martha  Morgan  for  technical  assistance, 
Vickie  Mayham  for  manuscript  preparation,  and  Erin 
Patrick  for  photography. 

REFERENCES 

1.  Han  BK,  Babcock  D,  McAdams  L,  et  al:  Bacterial  meningitis  in  infants: 
Sonographic  findings.  Radiology  1985;154(3):645-650. 

2.  Rosenberg  HK,  Levine  RS,  Stoltz  K,  et  al:  Bacterial  meningitis  in  infants: 
Sonographic  features.  AJNR  1983;4(3):822-825. 

3.  Reeder  JD,  Sanders  RC:  Ventriculitis  in  the  neonate:  Recognition  by  son- 
ography. AJNR  1983;4(1):37-41. 

4.  Hill  A,  Shakelford  GD,  Volpe  JJ,  et  al:  Ventriculitis  with  neonatal  bacterial 
meningitis:  Identification  by  real  time  ultrasound.  / Pediatr  1981;99(1):133- 
136. 

5.  Babcock  DS,  Han  BK:  Sonographic  recognition  of  gyral  infarction  in  men- 
ingitis. AJR  1985;  144(April): 833-836. 

6.  Fisher  RM,  Lipinski  JK:  Ultrasonograph  assessment  of  infectious  men- 
ingitis. Clin  Radiol  1984;35:267-273. 


Dr.  Gravois  is  a radiologist  affiliated  with  Earl  K.  Long  Memorial 
Hospital  in  Baton  Rouge.  She  is  also  an  instructor  in  radiology  at 
LSU  School  of  Medicine  in  New  Orleans. 


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34  JOURNAL  VOL  140  FEBRUARY 


GOLD-INDUCED  PNEUMONITIS 


BRUCE  A.  BAETHGE,  MD;  ROBERT  E.  WOLF,  MD,  PhD 


Gold-induced  pneumonitis  is  an  uncommon 
complication  of  chrysotherapy  in  rheumatoid 
arthritis  (RA).  Since  RA  patients  may  suffer  from  a 
variety  of  pulmonary  problems,  prompt  diagnosis 
is  essential  for  proper  management.  A report  of  a 
patient  with  gold-induced  pneumonitis  is 
presented  and  discussed. 


PULMONARY  COMPLICATIONS  are  common  in  rheu- 
matoid arthritis  (RA).  Pleuritis,  pulmonary  nod- 
ules, interstitial  fibrosis,  and  vasculitis  are  recognized 
features  of  the  disease.^  Patients  with  RA  also  develop 
frequent  pulmonary  infections  and  complications  of 
drug  therapy.^  When  RA  patients  present  with  pul- 
monary disease,  it  becomes  a challenging  problem  for 
the  clinician  to  establish  the  correct  diagnosis  and 
institute  proper  therapy. 

Gold-induced  pneumonitis  was  first  reported  in 
1948^  but  did  not  become  generally  recognized  until 
Winterbauer,  et  al  described  two  cases  with  lung  biop- 
sies in  1976.^  More  than  60  cases  have  subsequently 
been  reported  estabhshing  the  characteristic  clinical 
and  pathological  features  of  the  syndrome.^  Since  pul- 
monary toxicity  from  gold  therapy  is  uncommon,  it 


may  not  be  considered  or  recognized  when  rheu- 
matoid patients  initially  develop  respiratory  symp- 
toms. We  present  a case  which  demonstrates  the  char- 
acteristic clinical  features  of  the  syndrome  and  discuss 
the  etiology,  diagnosis,  and  management. 

CASE  REPORT 

A 73-year-old  white  woman  was  admitted  to  the  Uni- 
versity Hospital  at  LSU  Medical  Center  in  Shreveport 
on  Aug  1,  1985  for  evaluation  of  progressive  respi- 
ratory distress  and  nonproductive  cough.  One  year 
prior  to  admission,  she  had  developed  symmetrical 
polyarthritis  and  the  diagnosis  of  RA  was  established. 
When  symptoms  did  not  respond  to  non-steroidal 
anti-inflammatory  drugs,  intramuscular  chrysother- 
apy was  begun  on  March  20,  1985.  After  weekly  test 
doses  of  10  mg  and  25  mg,  she  received  50  mg  of 
aurothioglucose  weekly  until  the  date  of  admission 
(total  dose  835  mg).  In  early  July,  she  began  to  ex- 
perience wheezing  with  nonproductive  cough  and  was 
given  the  diagnosis  of  bronchitis.  Oral  ampidllin  was 
then  given  for  10  days  without  improvement. 

Her  past  medical  history  was  remarkable  for  mild 
chronic  obstructive  pulmonary  disease.  She  denied 
fever,  chills,  night  sweats,  or  pleuritic  pain.  The  only  ► 

JOURNAL  VOL  140  FEBRUARY  35 


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2900  West  Fork  Drive,  Suite  200,  Baton  Rouge,  LA  70827,  (504)  291-1807 


medication  she  had  routinely  received  before  admis- 
sion besides  gold  was  ibuprofen  600  mg  three  times 
each  day.  She  had  a history  of  cigarette  smoking  of 
a pack  a day  for  44  years  but  had  stopped  15  years 
ago.  A chest  roentgenogram  taken  in  March  1985  was 
read  as  "normal  for  age." 

Admission  physical  examination  revealed  a thin 
elderly  woman  using  accessory  muscles  with  breath- 
ing. Her  blood  pressure  was  128/70  mm  Hg,  pulse  80 
beats/min,  respiration  34/min;  she  was  afebrile.  Lung 
examination  revealed  diffuse  bilateral  wheezes.  Rales 
were  present  at  the  bases  with  dullness  to  percussion 
on  the  right  side.  Cardiac  examination  was  normal 
with  the  absence  of  any  murmur,  gallop,  or  rub.  The 
rest  of  the  physical  examination  was  essentially  nor- 
mal except  for  the  joint  findings  of  rheumatoid  ar- 
thritis. 

Admission  laboratory  studies  were  normal  except 
for  the  arterial  blood  gases.  There  was  marked  hy- 
poxia on  room  air  with  pH  7.41  PO2  40  mm  Hg,  PCO2 
49  mm  Hg,  and  O2  saturation  of  only  74%.  The  ad- 
mission chest  roentgenogram  revealed  bilateral  patchy 
infiltrates  and  pleural  effusions  (Fig  1).  Fluid  obtained 
by  thoracentesis  was  an  inflammatory  exudate  with 
a WBC  count  of  3,500  with  35%  polymorphonuclear 
leukocytes  and  65%  lymphocytes.  Smears  for  bacteria, 
mycobacteria,  and  fungi  were  negative  as  were  all 
cultures  and  serologic  tests  for  infection.  An  inter- 
mediate skin  test  for  tuberculosis  was  negative  with 
a positive  mumps  control. 

On  Aug  5,  1987,  a closed  needle  pleural  biopsy 
was  performed  on  the  right  side  which  revealed  only 
chronic,  non-specific  inflammation.  The  patient's 
symptoms  persisted  despite  treatment  with  bron- 
chodilators  and  supplemental  oxygen.  On  Aug  15, 
1987,  she  underwent  an  open  biopsy  of  the  right  lung. 
The  histopathology  revealed  numerous  giant  cells, 
foamy  histiocytes,  and  interstitial  fibrosis  with  some 
lipid  deposits  in  the  interstitial  spaces.  The  biopsy  was 
interpreted  as  representing  an  organizing  pneumo- 
nitis. All  stains  for  bacteria,  mycobacteria,  and  fungi 
were  negative.  Based  on  the  clinical  history  and  path- 
ologic findings,  a diagnosis  of  gold  pneumonitis  was 
made.  Chrysotherapy  was  discontinued.  The  patient 
was  started  on  prednisone  40  mg/day  and  experi- 
enced dramatic  improvement  in  symptoms.  Spi- 
rometry obtained  Aug  22,  1987  revealed  severe  re- 
strictive disease  with  a forced  expiratory  volume  at 
one  second  of  0.59  L (34%  of  predicted)  and  with  a 


Fig  1.  Chest  roentgenogram  revealing  bilateral 
patchy  infiltrates  and  pleural  effusions. 


forced  vital  capacity  of  0.9  L (36%  of  predicted);  with 
the  reduced  flow  rate  compatible  with  mild  obstruc- 
tive ventilating  impairment.  By  Aug  23,  1987,  the  pa- 
tient was  improved  enough  for  discharge. 

Frequent  outpatient  examinations  documented 
improvement  of  respiratory  symptoms  and  arterial 
blood  gas  determinations.  The  prednisone  was  grad- 
ually tapered  over  the  next  four  months.  A repeat 
chest  roentgenogram  on  Nov  20,  1986  (Fig  2)  revealed 
only  residual  interstitial  changes.  All  pulmonary 
symptoms  had  resolved. 

DISCUSSION 

Gold-induced  pneumonitis  is  an  uncommon  disorder 
with  an  incompletely  understood  pathogenesis.  A re- 
cent article  reviewing  a 47-year  experience  with  gold 
therapy  in  1,019  rheumatoid  patients  did  not  describe 
a single  case.^  A multicenter  study  from  Finland  iden- 
tified 16  cases  of  gold-induced  pneumonitis  over  a 10- 


JOURNAL  VOL  140  FEBRUARY  37 


Fig  2.  Repeat  chest  roentgenogram  revealing  re- 
siduai  interstitiai  changes. 


year  period.^  The  syndrome  usually  occurs  with  the 
injectable  gold  salts,  gold  sodium  thiomalate  or  au- 
rothioglucose;  however,  there  is  one  report  of  a case 
with  the  oral  preparation  auranofin/  While  there  is 
no  way  to  predict  which  patients  are  at  risk,  there  is 
evidence  that  genetic  factors  may  contribute  to  the 
development  of  gold  pneumonitis.  Partanen,  et  al  have 
found  that  patients  with  RA  and  gold  pneumonitis 
express  two  extended  human  lymphocyte  antigen 
haplotypes  in  higher  frequencies  than  controls.®  The 
clinical  manifestations  and  pathological  findings  of 
the  syndrome  strongly  suggest  that  it  is  a hypersen- 
sitivity reaction  to  gold  and  not  a feature  of  rheu- 
matoid disease.  This  concept  is  supported  by  reports 
of  cases  of  gold  pneumonitis  occurring  in  patients 
with  osteoarthritis  erroneously  treated  with  gold.^  The 
syndrome  also  has  recurred  when  patients  were  re- 
challenged with  gold.®  Although  pathogenesis  of  the 


lung  injury  has  not  been  studied  extensively,  gold- 
stimulated  peripheral  blood  lymphocytes  from  pa- 
tients with  gold  pneumonitis  elaborate  lymphokines 
and  chemotactic  factors,^  suggesting  that  cell-  mediated 
immunity  may  play  a role. 

The  characteristics  of  patients  with  gold-induced 
pneumonitis  have  been  described  in  a recent  review. 
The  individuals  are  usually  women  with  the  mean 
age  of  53,  who  had  received  an  average  of  582  mg  of 
gold  (range  120  mg  to  1660  mg)  before  symptoms 
appeared.  Dyspnea  on  exertion  has  been  the  pre- 
senting complaint  in  95%  of  patients,  while  less  than 
half  of  the  patients  will  present  with  cough  or  fever. 
Other  complications  of  gold  therapy  are  usually  ab- 
sent although  gold  dermatitis  has  appeared  with  pul- 
monary symptoms  in  some  patients.^®  Physical  ex- 
amination usually  reveals  only  tachypnea  and  crepitant 
basilar  rales.  The  chest  roentgenographic  findings  are 
non-specific  with  diffuse,  usually  bilateral,  interstitial 
and/or  alveolar  infiltrates  present  together  with  patchy 
consolidations. 

There  are  no  characteristic  laboratory  findings. 
Peripheral  blood  leukocytosis  and  eosinophilia  are 
found  in  only  about  half  of  the  patients.  Serologic 
studies  are  not  helpful.  The  erythrocyte  sedimenta- 
tion rate  is  usually  elevated,  and  59%  of  the  patients 
have  been  positive  for  rheumatoid  factor.  There  is  one 
report  of  hypogammaglobulinemia  occurring  with  gold 
pneumonitis.^^  The  majority  of  patients  have  arterial 
blood  gas  abnormalities  with  hypoxia  and  hypocarbia 
being  common.  There  is  a report  of  ventilatory  failure 
with  hypercarbia.^°  Pulmonary  function  testing  has 
consistently  demonstrated  a restrictive  ventilatory 
pattern  with  reduced  single  breath  carbon  monoxide 
diffusion  capacity.  Serial  pulmonary  function  testing 
has  shown  improvement  in  the  restrictive  defect  after 
withdrawal  of  gold  and  initiation  of  glucocorticoid 
therapy. 

The  most  common  pathologic  finding  in  the  lung 
can  be  described  as  fibrosing  alveolitis.  Differing  pat- 
terns of  alveolar  inflammation  with  infiltration  of  lym- 
phocytes, plasma  cells,  and  histiocytes  and  interstitial 
fibrositis  have  been  reported.^®  Reactive  type  II  alveo- 
lar cell  hyperplasia  occurs  and  can  be  prominent 
enough  to  initially  suggest  the  diagnosis  of  malig- 
nancy.^® In  one  patient,  indirect  immunofluorescence 
has  demonstrated  subepithelial  deposits  of  IgG,  and 
scanning  electon  microscopy  has  demonstrated  gold 


38  JOURNAL  VOL  140  FEBRUARY 


deposits. Unfortunately  the  histologic  findings  are 
not  diagnostic  for  gold  pneumonitis  since  all  of  the 
changes  described  can  be  found  with  primary  rheu- 
matoid lung  disease. 

The  differential  diagnosis  of  gold  pneumonitis 
includes  primary  rheumatoid  lung  disease,  chronic 
pulmonary  infection,  and  malignancy.  The  latter  two 
diagnoses  can  usually  be  excluded  by  negative  stains 
and  cultures  for  pathogens  and  by  tissue  histopath- 
ology.  Since  the  pathologic  appearance  of  gold- 
induced  pneumonitis  can  be  similar  to  rheumatoid 
interstitial  lung  disease,  the  clinician  must  rely  on 
clinical  features  and  suspicion  to  make  the  diagnosis. 

Recently,  the  use  of  bronchoalveolar  lavage  (BAL) 
has  been  advocated  for  diagnosis. Evaluation  of  the 
lavage  fluid  from  gold  pneumonitis  patients  reveals 
an  increased  number  of  lymphocytes  compared  to 
normal  controls  while  increased  numbers  of  poly- 
morphonuclear leukocytes  are  usually  found  in  pri- 
mary rheumatoid  interstitial  lung  disease.^  Although 
this  technique  appears  promising,  the  clinical  use- 
fulness of  BAL  in  gold-induced  pneumonitis  remains 
to  be  established. 

The  most  useful  diagnostic  and  therapeutic  ma- 
neuver is  observation  of  the  patient  after  stopping 
gold.  The  diagnosis  can  usually  be  made  when  the 
following  criteria  are  found:  acute  to  subacute  onset 
of  symptoms  during  early  stages  of  gold  therapy;  dif- 
fuse usually  bilateral  pulmonary  infiltrates;  improve- 
ment after  discontinuation  of  gold,  treatment  with 
steroids  or  both;  and  no  recurrence  of  the  disease  in 
follow-up.  These  features  allow  differentiation  from 
rheumatoid  interstitial  lung  disease  which  usually  is 
slow  to  develop  and  does  not  improve  dramatically 
with  therapy. 

Some  patients  require  no  treatment  other  than 
discontinuation  of  chrysotherapy.  Often  patients  do 
have  persistent  or  severe  symptoms  that  require 
administration  or  glucocorticoids^^  since  gold  can  re- 
main in  lung  tissue  for  weeks  after  cessation  of  ther- 
apy.^ With  administration  of  glucocorticoids,  im- 
provement will  occur  rapidly  in  most  patients.  The 
dose  of  glucocorticoids  and  duration  of  therapy  is 
dependent  upon  the  clinical  response  of  the  patient. 
It  has  not  been  proven,  but  seems  reasonable,  that 
prompt  diagnosis  and  therapy  will  lessen  the  chances 
of  developing  irreversible  fibrosis.  The  syndrome  has 
been  fatal  for  some  patients. 


CONCLUSIONS 

Gold  toxicity  must  be  considered  when  rheumatoid 
arthritis  patients  develop  pulmonary  disease.  Al- 
though uncommon,  gold  pneumonitis  may  be  fatal 
or  lead  to  pulmonary  fibrosis  if  not  recognized  and 
managed  promptly.  The  characteristic  features  of  acute 
or  subacute  pneumonitis  occurring  in  a patient  re- 
ceiving gold  should  alert  clinicians  to  the  possibility 
of  the  disorder.  Aggressive  diagnostic  pulmonary 
procedures  to  exclude  infection  or  malignancy  and 
withholding  gold  therapy  will  usually  allow  the  di- 
agnosis to  be  established.  Treatment  with  glucocor- 
ticoids may  be  necessary  for  some  patients.  ■ 

REFERENCES 

1.  Shiel  WC,  Prete  PE:  Pleuropulmonary  manifestations  of  rheumatoid  ar- 
thritis. Semin  Arthritis  Rheum  1984;13:235-243. 

2.  Savilahti  M:  Pulmonary  complications  following  use  of  gold  salts.  Ann 
Med  Intern  Fenn  1948;37:263-266. 

3.  Winterbauer  RH,  Wilke  KR,  WheeUs  RF:  Diffuse  pulmonary  injury  as- 
sociated with  gold  treatment.  N Engl  J Med  1976;294:919-921 . 

4.  Evans  RB,  Ettensohn  DB,  Fawaz-Estrup  F,  et  al:  Gold  lung:  Recent  de- 
velopments in  pathogenesis,  diagnosis  and  therapy.  Semin  Arthritis  Rheum 
1987;16:196-205. 

5.  Lockie  LM,  Smith  DM:  Forty-seven  years  experience  with  gold  therapy 
in  1,019  rheumatoid  arthritis  patients.  Semin  Arthritis  Rheum  1985;14:238- 
246. 

6.  Kala  MH,  Van  Assendelft  AFIW,  Ilonen  J,  et  al:  Association  of  different 
HLA  antigens  with  various  toxic  effects  of  gold  salts  in  rheumatoid 
arthritis.  Ann  Rheum  Dis  1986;45:177-182. 

7.  Davis  P,  Menard  H,  Thompson  J,  et  al:  One  year  comparative  study  of 
gold  sodium  thiomalate  and  auranofin  in  the  treatment  of  rheumatoid 
arthritis.  J Rheumatol  1985;12:60-67. 

8.  Partanen  J,  Van  Assendelft  AHW,  Koskimies  S,  et  al:  Patients  with  rheu- 
matoid arthritis  and  gold-induced  pneumonitis  express  two  high-risk 
major  histocompatabUity  complex  patterns.  Chest  1987;92:277-281. 

9.  McCormick  J,  Cole  S,  Lahirir  B,  et  al:  Pneumonitis  caused  by  gold  salt 
therapy:  Evidence  for  the  role  of  cell-mediated  immunity  in  its  patho- 
genesis. Am  Rev  Respir  Dis  1980;122:145-152. 

10.  Cooke  N,  Bamji  A:  Gold  lung.  Rheumatol  Rehabil  1981;20:129-135. 

11.  Stuckey  BGA,  Hanrahan  PS,  Zilko  PJ,  et  al:  HypoganunaglobulLnemia 
and  lung  infiltrates  after  gold  therapy.  / Rheumatol  1986;13:468-469. 

12.  Levinson  ML,  Lynch  JP,  Bower  JS:  Reversal  of  progressive  life  threat- 
ening gold  hypersensitivity  pneumonitis  by  corticosteroids.  Am  f Med 
1981;71:908-912. 

13.  James  DW,  Whimster  WF,  Hamilton  EBD:  Gold  Itmg.  BrMed  J 1978;1:1523- 
1524. 

14.  Yousem  SA,  Colby  TV,  Carrington  CB:  Lung  biopsy  in  rheumatoid  ar- 
thritis. Am  Rev  Respir  Dis  1985;131:770-777. 

15.  Ettensohn  DB,  Robots  NJ,  Condemi  JJ:  Bronchoalveolar  lavage  in  gold 
lung.  Chest  1984;85:569-570. 

16.  Scharf  J,  Nahir  M,  Kleinhaus  U,  et  al:  Diffuse  pulmonary  injiuy  asso- 
ciated with  gold  therapy.  JAMA  1977;237:2412-2414. 


Drs.  Baethge  and  Wolf  are  from  the  Section  of  Rheumatology,  Dept  of 
Medicine  at  LSU  Medical  Center  in  Shreveport. 

Requests  for  reprints  should  be  sent  to  Bruce  A.  Baethge,  MD, 
LSUMC-S,  Box  33932,  Shreveport,  LA  71130;  (318)  674-5930. 

JOURNAL  VOL  140  FEBRUARY  39 


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OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY  March  1988 


Ycedin^  practices  of  loio-iucomc  infants:  A Ncio  Orleans  Health  Department  Study 


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Established  1844.  Owned  and  edited  by  The 
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VOLUME  140  / NUMBER  3 / MARCH 


ARTICLES 

3 

Schedule  of  Events  for 
the  108th  Annual 
Meeting 

Hosea  J.  Doucet,  MD,  MPH 
Roy  A.  Berry 

16 

Feeding  practices  of 
low^-income  infants: 

A New  Orleans 
Health  Department  Study 

Neil  H.  Baum,  MD 

27 

Treatment  of  impotence: 
Nonsurgical  modalities 

Nicholas  J.  Persich 
Edward  I.  Bluth,  MD 

35 

Evaluation  of 
extravasation  during 
intravenous  urography 

DEPARTMENTS 

2 

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5 

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13 

Otolaryngology /Head 

& Neck  Surgery  Report 

32 

Books  Received 

45 

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jOURNALS 

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use  during  surgery.  Am  / Clin  Pathol  1979;71 :680-692. 

BOOKS 

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Norton  W.  Voorhies,  MD,  Editor 


ECG  OF  THE  MONTH 


SHORT-CUTS 

JORGE  I.  MARTINEZ-LOPEZ,  MD 


The  12-lead  ECG  shown  below  belongs  to  a 44-year-old  man  with  documented  paroxysms  of  supraven- 
tricular tachycardia.  He  was  on  no  medications. 


What  is  your  diagnosis?  Elucidation  is  on  page  6. 


JOURNAL  VOL  140  MARCH  5 


ECG  of  the  Month 

Case  presentation  is  on  page  5. 

DIAGNOSIS  — Ventricular  preexcitation 

The  basic  rhythm  is  sinus  at  75  times  a minute.  The 
PR  interval  is  extremely  short  (0.08  sec)  and  no  PR 
segment  is  inscribed.  QRS  complexes  are  narrow  (0.08 
to  0.09  sec)  and  are  associated  with  non-specific  ST 
segment  and  T wave  changes  in  leads  1,  2,  AVF,  and 
V3  through  V6.  The  R waves  in  the  precordial  leads 
are  of  large  amplitude.  There  is  an  early  transition 
zone  of  the  QRS  complexes  in  the  precordial  leads. 

The  combination  of  short  PR  interval  and  narrow 
QRS,  in  a patient  who  has  had  paroxysms  of  supra- 
ventricular tachycardia,  is  consistent  with  a diagnosis 
of  a ventricular  preexcitation  syndrome,  and  will  be 
the  subject  of  the  discussion  to  follow. 

DISCUSSION 

To  understand  ventricular  preexcitation,  it  is  impor- 
tant to  recall  several  basic  facts.  First,  the  atrioven- 
tricular rings  and  sulci  are  impenetrable  to  electrical 
impulses  originating  in  either  the  atria  or  the  ventri- 
cles. Second,  electrical  impulses  generated  in  the  sinus 
node  or  atria  normally  can  propagate  into  the  ven- 
tricles only  by  engaging  and  crossing  the  AV  node 
and  bundle  of  His.  Third,  the  AV  junctional  area  is 
that  portion  of  the  cardiac  conducting  system  re- 
sponsible for  the  delay  in  the  passage  of  supraven- 
tricular impulses  into  the  distal  conducting  system  of 
the  heart.  In  the  normal  heart,  therefore,  sinus  im- 
pulses first  depolarize  the  atria  and,  on  their  journey 
toward  the  ventricles,  are  slowed  down  at  the  AV 
junctional  area.  Upon  exiting  from  the  AV  junctional 
area,  the  advancing  electrical  fronts  propagate  rapidly 
down  the  bundle  of  His  to  both  bundle  branches, 
resulting  in  near-simultaneous  depolarization  of  both 
ventricles.  This  sequence  of  events  is  depicted  on  the 
surface  ECG  by  P-QRS-T  cycles.  The  PR  interval, 
measured  from  the  onset  of  the  P wave  to  the  first 
deflection  of  the  QRS  complex,  ranges  from  0.12  to 
0.20  seconds  in  the  adult  healthy  subject. 

Ventricular  preexcitation  (VPE)  is  said  to  be  ''pres- 
ent when,  in  relation  to  the  atrial  events,  the  whole 
or  part  of  the  ventricular  myocardium  is  activated  by 
the  impulse  originating  in  the  atrium  earlier  than 

6 JOURNAL  VOL  140  MARCH 


would  be  expected  if  the  impulse  reached  the  ven- 
tricles by  way  of  the  normal  specialized  conducting 
system  alone."  Based  on  this  definition,  it  is  logical 
to  conclude  that,  for  VPE  to  occur,  advancing  supra- 
ventricular impulses  must  take  a "short-cut"  to  acti- 
vate parts  or  all  of  the  ventricular  musculature  earlier 
than  expected.  These  "short-cuts"  are  designated  as 
accessory  pathways  (AP). 

Some  APs  have  been  shown  to  exist,  whUe  others 
are  only  hypothetical.  Among  APs  considered  to  be 
responsible  for  VPE  are  the  following:  connections 
originating  in  atrial  myocardium  and  inserting  in  the 
corresponding  ventricle  (bundles  of  Kent)  or  origi- 
nating in  the  AV  node  and  inserting  in  the  ventricle 
(Paladino  tracts);  bypass  tracts  originating  in  atrial 
muscle  and  inserting  in  the  penetrating  bundle  of  His 
(atriofascicular  tracts);  and  connections  between  the 
distal  intraventricular  conducting  system  and  the  ven- 
tricle (fasciculoventricular  connections  or  paraspecific 
fibers  of  Mahaim).  Still  hypothetical  are  intranodal 
bypass  tracts  and  AV  nodal  malformations  that  would 
eliminate  AV  junctional  conduction  delay.  Given  the 
presence  of  these  potential  ports  of  entry  into  the 
ventricular  muscle,  supraventricular  impulses  can  de- 
polarize the  ventricles  in  several  ways:  entirely  by  way 
of  the  normal  cardiac  conducting  system;  entirely  by 
way  of  AP;  or  over  both  pathways  simultaneously. 
The  locations  and  number  of  existing  APs  and  their 
functional  status  will  determine  whether  or  not  ECG 
findings  are  present  and,  when  present,  their  char- 
acteristic features. 

Recognition  of  VPE  on  the  surface  ECG  is  achieved 
primarily  by  measurement  of  the  PR  interval  and  the 
duration  of  the  QRS  complexes  and  by  examining  the 
QRS  configuration.  Three  major  electrocardiographic 
patterns  are  recognized  during  sinus  rhythm.  In  the- 
classic  Woljf -Parkinson-White  pattern,  the  PR  interval  is 
short  (less  than  0.12  sec),  the  QRS  is  prolonged  (more 
than  0.10  sec),  a slurred  initial  deflection  of  the  QRS 
is  present  (delta  wave),  and  the  P-J  interval  is  normal. 
The  pattern  of  the  so-called  Lown-Ganong-Levine  syn- 
drome includes  a PR  shorter  than  0.11  sec  and  narrow 
QRS  complexes.  The  third  ECG  pattern  of  VPE  is 
attributed  to  the  presence  of  paraspecific  fibers  of  Ma- 
haim and  consists  of  a normal  PR  interval  and  a QRS 
longer  than  0.10  sec  with  a delta  wave.  Variants  of 
these  three  major  patterns  have  been  described. 

Recognition  of  VPE  is  important  for  two  main 


reasons.  The  first  is  that  patients  with  VPE  patterns 
are  prone  to  develop  tachycardias.  Most  of  the  tach- 
ycardias observed  in  patients  with  VPE  are  reentrant 
and  involve  the  normal  conduction  system  of  the  heart 
and  the  AP.  Less  often,  paroxysmal  atrial  fibrillation 
or  flutter  is  associated  with  rapid  antegrade  conduc- 
tion over  the  AP  (innocent  bystander  tachycardia). 
The  second  reason  is  that  VPE  patterns  on  the  ECG 
may  mimic  other  cardiac  pathologies.  Patients  with 
VPE  who  develop  atrioventricular  reentrant  tachy- 
cardias are  said  to  have  VPE  syndrome. 

In  the  tracing  shown  here,  the  PR  interval  is  so 
short  (0.08  sec)  that  the  PR  segment  is  not  recorded 
and  the  QRS  complex  is  narrow  (0.09  sec).  The  com- 
bination of  short  PR  interval  and  narrow  QRS  and  the 
history  of  recurrent  paroxysms  of  PSVT  in  this  patient 
might  be  construed  as  favoring  the  diagnosis  of  Lown- 
Ganong-Levine  syndrome.  However,  close  exami- 


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nation  of  the  QRS  complexes,  particularly  in  leads  2, 
AVF,  and  V3  through  V6,  discloses  the  presence  of  a 
small  delta  wave  in  those  leads.  For  this  reason,  it  is 
more  likely  that  the  tracing  represents  an  “incom- 
plete" form  of  Wolf f-Parkinson- White  syndrome.  This 
finding  brings  into  sharp  focus  one  last  important 
point:  it  is  erroneous  to  think  that  the  Wolff-Parkin- 
son-White  syndrome  pattern  is  always  associated  with 
a wide  QRS.  Because  the  resulting  QRS  complexes 
during  sinus  rhythm  in  patients  with  bundles  of  Kent 
are  fusion  complexes,  all  gradations  of  fusion  can  occur 
depending  on  how  much  of  the  advancing  sinus  front 
takes  a short-cut  by  way  of  the  AP  and  how  much  of 
it  travels  antegrade  in  the  normal  conducting  system. 

■ 

SELECTED  REFERENCES 

1.  Massumi  RA,  Vera  Z:  Patterns  and  mechanisms  of  QRS  normalization  in 
patients  with  Wolff-Parkinson- White  syndrome.  Am  J Cardiol  1971;28:541- 
554. 

2.  Wiener  I:  Syndromes  of  Lown-Ganong-Levine  and  enhanced  atrioven- 
tricular nodal  conduction.  Am  J Cardiol  1983;52:637-639. 

3.  Khair  Gl,  Tristani  FE,  Barrvrah  VS:  Dynamic  variations  in  Wolff-Parkinson- 
White  syndrome:  Electrocardiographic  and  clinical  observations.  Am  Heart 
J 1983;105:878-882. 

4.  Prystowsky  EN,  Miles  WM,  Heger  }J,  et  al:  Preexcitation  syndromes.  Med 
Clin  North  Am  1984;68:831-893. 

5.  Giorgi  C,  Ackaoui  A,  Nadeau  R,  et  al:  Wolff-Parkinson-White  VCG  pat- 
terns that  mimic  other  cardiac  pathologies:  A correlative  study  with  the 
preexcitation  pathway  localization.  Am  Heart  J 1986;111:891-902. 


Dr.  Martinez-Lopez  is  a specialist  in  cardiovascular  diseases  affiliated 
with  the  Cardiology  Service,  Dept  of  Medicine  at  William  Beaumont 
Army  Medical  Center  in  El  Paso,  TX. 

The  opinions  and  assertions  contained  herein  are  the  private  views  of  the 
author  and  not  to  be  construed  as  official  or  as  reflecting  the  views  of 
the  Dept  of  the  Army  or  Dept  of  Defense. 


JOURNAL  VOL  140  MARCH  7 


CALENDAR 


April 


April  8-10 

Louisiana  Psychiatric  Association/Mississippi  Psychiatric 
Association  Joint  Meeting,  Natchez,  Mississippi.  Contact: 
Charlene  Smith,  Louisiana  Psyciatric  Association,  PO  Box  15765, 
New  Orleans,  LA  70175;  (504)891-1030. 

April  9 

Selected  Topics  in  Infectious  Diseases,  Miramar  Sheraton 
Hotel,  Santa  Monica,  CA.  Contact:  Beth  Hill,  UCLA  Extension, 
PO  Box  24901,  Los  Angeles,  CA  90024-0901;  (213)825-1901. 

April  13-16 

Comprehensive  Review  Course  in  Hand  Surgery,  Chicago. 
Contact:  American  Society  for  Surgery  of  the  Hand,  3025  South 
Parker  Rd,  Suite  65,  Aurora,  CO  80014;  (303)755-4588. 

April  13-17 

4th  Annual  Family  Medicine  Review,  Austin,  Texas,  Con- 
tact: Dept  of  Continuing  Medical  Education,  Scott  & White,  2401 
South  31st  St,  Temple,  TX  76508;  (817)774-2350. 

April  14-16 

National  Cocaine  Conference:  Clinical  Advances  in  Treat- 
ment, Recovery  & Relapse  Prevention,  Orlando,  Florida. 
Contact:  US  Training  Journal  Inc,  National  Cocaine  Conference, 
1721  Blount  Rd,  Suite  1,  Pompano  Beach,  FL  33069; 
(800)851-9100. 

April  14-17 

Controversies  in  the  Management  of  Skin  Tumors,  Kiawah 
Island  Resort,  South  Carolina.  Contact:  Plastic  Surgery  Educa- 
tional Foundation,  233  N Michigan  Ave,  Suite  1900,  Chicago,  IL 
60601,  (312)856-1818. 

April  16-17 

Workshop  on  Transplantation,  Pittsburgh.  Contact:  American 
Society  of  Anesthesiologists,  515  Busse  Hwy,  Park  Ridge,  IL  60068. 

April  20-24 

Critical  Care  Medicine  1988:  2nd  Annual  Review  and  Up- 
date Course,  Arlington,  VA.  Contact:  Svetlana  Lisanti,  Center 
for  Bio-Medical  Communication,  491  Grand  Ave,  Englewood,  NJ 
07631;  (201)385-1808. 

April  22-23 

2nd  Annual  Facial  Fracture  Surgery,  Doubletree  Hotel, 
Atlanta.  Contact:  Richard  A.  Pollock,  MD,  Georgia  Baptist 
Medical  Center,  Box  95,  300  Boulevard  NE,  Atlanta,  GA  30312; 
(404)355-9266. 


April  22-24 

3rd  International  Interdisciplinary  Conference  on  Hyperten- 
sion in  Blacks,  Baltimore.  Contact:  Cecile  Cate,  Conference  Coor- 
dinator, International  Society  on  Hypertension  in  Blacks,  69  Butler 
St  SE,  Atlanta,  GA  30303;  (404)589-3810. 

April  23-24 

The  Cutting  Edge  1988/Innovations  in  Psychotherapy:  Help- 
ing Individuals  and  Couples  to  Change,  Hotel  Del  Cor- 
onado, San  Diego.  Contact:  Office  of  Continuing  Medical  Educa- 
tion, UC  San  Diego  School  of  Medicine,  La  Jolla,  CA  92093; 
(619)534-3940. 

April  27-30 

Tendon  and  Soft  Tissue  Injuries  of  the  Hand,  The  Cottages 
Resort,  Hilton  Head,  South  Carolina.  Contact:  American  Society 
for  Surgery  of  the  Hand,  3025  South  Parker  Rd,  Suite  65,  Aurora, 
CO  80014;  (303)755-4588. 


May 


May  2-4 

NIH  Consensus  Development  Conference:  Cochlear  Im- 
plants, Bethesda,  Maryland.  Contact:  Conference  Registrar,  Pro- 
spect Associates,  Suite  500,  1801  Rockville  Pike,  Rockville,  MD 
20852;  (301)468-MEET. 

May  4-6 

6th  Regions  II  & III  High  Blood  Pressure  Conference/New 
Challenges  — Creative  Solutions,  Richmond,  Virginia.  Con- 
tact: Paula  A.  Ciaverella  or  Joann  T.  Richardson,  Virginia  Dept 
of  Health,  Division  of  Chronic  Disease  Control,  109  Governor  St, 
Madison  Bldg,  Richmond,  VA  23219;  (804)786-4065. 

May  5-7 

The  National  Conference  on  Health  Care  Leadership  and 
Management,  Sheraton  Harbor  Island,  San  Diego.  Contact: 
Sherry  Mason,  American  Academy  of  Medical  Directors,  4830  W 
Kennedy  Blvd,  Suite  648,  Tampa,  FL  33609-2517;  (813)287-2000. 

May  7 

Perspectives  in  Rheumatology,  Century  City,  CA.  Contact: 
Beth  Hill,  UCLA  Extension,  PO  Box  24901,  Los  Angeles,  CA 
90024-0901;  (213)825-1901. 

May  13  - June3 

Cruise /Seminar  on  Risk  Management  and  Comparative 
Medicolegal  Issues,  Hong  Kong,  China,  and  Japan.  Inter- 
national Conferences,  Suite  C,  189  Lodge  Ave,  Huntington  Sta- 
tion, NY  11746;  (800)521-0076,  (516)549-0869. 


8 JOURNAL  VOL  140  MARCH 


OTOLARYNGOLOGY/ 

HEAD  & NECK  SURGERY  REPORT 


LYMPHANGIOMA  OF  THE  NECK 
IN  INFANTS  AND  CHILDREN 


HENRY  A.  MENTZ  III,  MD;  HOMER  D.  GRAHAM  III,  MD; 

PAUL  BLAIR,  MD 


Lymphangiomas  are  benign  congenital  lymphatic 
malformations  found  in  childhood.  There  is  a 
predilection  for  the  head  and  neck  creating 
difficult  challenges  in  management  decisions.^ 
Provided  is  a brief  description  of  the  pathogenesis 
of  this  disease  and  a review  of  the  treatment 
options.  We  present  a case  report  that  illustrates  a 
practical  surgical  solution  in  the  management  of  a 

life  threatening  situation. 


i 

y 

I 


Lymphangiomas  are  uncommon  benign  congenital 
lymphatic  tumors  which  present  difficult  man- 
agement decisions.  This  tumor  was  originally  de- 
scribed by  Redenbacker  in  1828  and  by  Wernher^  in 
1843  as  a cystic  tumor  occurring  in  certain  sites  of  the 
body  with  predilection  for  the  head  and  neck.  Further 
description  of  these  largely  cystic  tumors  over  the  last 
century  parallels  the  description  of  lymphatic  devel- 
opment. Furthermore,  the  terms  lymphangioma  and 
cystic  hygroma  have  been  used  interchangeably  al- 
though, from  a histological  standpoint,  lymphan- 
gioma is  a better  term. 

ETIOLOGY 

There  is  some  controversy  regarding  the  precise  etiol- 
ogy of  this  tumor.  The  most  plausible  theory  was  first 
presented  in  1913  by  Dowd.^  It  is  thought  that  these 
tumors  arise  from  sequestered  portions  of  embryonic 
lymph  sacs  and  the  accumulation  of  lymph  causes 
pressure  atrophy  and  invasion  into  surrounding 
structures. 

PRESENTATION 

The  incidence  of  this  congenital  tumor  is  uncommon. 

JOURNAL  VOL  140  MARCH  13 


A total  of  40%  of  these  congenital  tumors  appear  in 
the  newborn  and  80%  to  90%  have  developed  by  the 
second  year  of  life.  The  appearance  of  these  tumors 
beyond  puberty  is  extremely  rare.  There  is  a very 
slightly  increased  incidence  in  males  and  in  occur- 
rence on  the  right.  Almost  half  of  these  tumors  occur 
in  the  head  and  neck  regions.  The  neck  is  the  single 
most  common  involved  structure. 

The  presentation  of  this  tumor  is  characteristi- 
cally a painless  soft  swelling  or  mass  in  the  neck.  The 
larger  lesions  may  be  multilobulated,  irregular,  com- 
pressible, and  easUy  transLlluminated.  Tenderness  may 
indicate  infection.  A sudden  increase  in  size  may  be 
due  to  hemorrhage.  Dyspnea  and  dysphagia  indicate 
tumor  encroachment  on  respiratory  or  food  passage- 
ways. 

The  differential  diagnosis  includes  branchial  cleft 
cysts,  thyroglossal  duct  cysts,  dermoid  cysts,  foregut 
cysts,  rare  malignant  tumors,  deep  hemangiomas, 
cervical  infections,  lipomas,  and  ranulas.  The  workup 
should  include  a careful  history  and  examination  with 
special  emphasis  on  the  airway  and  deglutition.  En- 
doscopic examination  can  provide  valuable  insight  to 
the  extent  of  the  tumor.  Lymphangiomas  can  involve 
the  hypopharynx  and  larynx.  Roentgenograms  will 
provide  little  information  except  that  of  airway  en- 
croachment or  displacement.  Injection  of  opaque  ma- 
terial is  mentioned  only  to  be  discouraged  because 
cysts  do  not  often  communicate  and  because  infec- 
tions within  these  cysts  are  poorly  tolerated.  Com- 
puted tomographic  scans  and  magnetic  resonance  im- 
aging will  provide  useful  information. 

Farber  and  Landing^  have  demonstrated  four  his- 
tologic types:  cystic,  cavernous,  capillary,  and  he- 
mangiolymphangioma  types.  The  cavernous  lym- 
phangioma is  the  most  frequent  and  presents  the 
greatest  management  problem.  Controversy  exists  in 
histologic  typing  because  there  is  no  sharp  dividing 
line  between  these  four  groups.  Frequently  there  is  a 
combination  of  these  types  found  in  one  patient.  Fur- 
thermore, there  is  some  evidence  that  there  is  a change 
from  capillary  to  cavernous  to  cystic  type  as  the  dis- 
ease progresses. 


MANAGEMENT 

The  treatment  goals  and  principles  are  universal  and 
include  early  treatment,  resolution  of  the  entire  tu- 
mor, the  return  of  function  to  the  involved  structures, 
the  relief  of  functional  complications  and  emotional 
consequences,  and  a good  cosmetic  result.^  Manage- 
ment options  include  a wide  variety  of  practices  and 
procedures.  Observation  is  a dangerous  approach  be- 
cause spontaneous  resolution  rarely  occurs  and  le- 
sions undergo  growth  and  expansion  which  may  lead 
to  more  difficult  treatment.  Surgeons  once  favored 
aspiration,  which  rarely  resulted  in  permanent  cure. 
Complications  included  infection  and  hemorrhage 
within  the  cyst  leading  to  further  expansion.  Aspi- 
ration is  useful  for  emergency  decompression  pre- 
ceding surgical  cure.  A small  unilocular  cystic  lym- 
phangioma may  respond  to  palliative  treatment  such 
as  aspiration  or  incision  and  drainage,  but  it  is  oth- 
erwise not  useful.  Various  sclerosing  agents  have  in- 
cluded morrhuate  sodium,  boiling  water,  quinine,  ur- 
ethan,  saturated  saline,  and  25%  glucose.  The  pitfalls 
of  sclerosing  agents  have  included  damage  to  adjacent 
structures  with  fibrosis,  thickening,  and  infection. 
These  may  create  difficulty  in  surgical  removal  often 
leading  to  failure.  These  agents  are  rarely  used  except 
in  cases  of  residual  tumor  left  behind.  However,  in 
these  cases  unroofing  of  the  cysts  is  a more  desirable 
alternative.^  Steroids  have  been  used  effectively  in  the 
treatment  of  hemangiomas;  however,  they  have  not 
proved  useful  in  the  treatment  of  lymphangioma.  Ir- 
radiation, advocated  in  the  past,  provided  occasional 
cures,  but  failures  were  common.  Also,  irradiation 
produced  damage  to  other  structures  with  potential 
induction  of  malignancies,  potential  for  local  growth 
retardation,  cosmetic  deformity,  infection,  and  death. 

Surgery  has  been  deemed  the  treatment  of  choice 
for  lymphangioma.  A primary  concern  in  manage- 
ment must  be  constant  maintenance  of  a patent  air- 
way: tracheostomy  may  be  necessary  in  this  case. 
Other  considerations  include  deglutition  and  nerve 
function.  Most  authors  recommend  complete  excision 
if  possible.  Vital  structures  should  be  preserved  even 
at  the  expense  of  incomplete  excision.  The  most  dif- 
ficult head  and  neck  tumors  involve  the  eyelids,  max- 
illa, and  mandible.  In  these  areas,  many  times,  the 
tumors  are  removed  in  staged  procedures.  When  gross 


14  JOURNAL  VOL  140  MARCH 


tumor  was  completely  excised  the  recurrence  rate  was 
in  the  area  of  30%  and  when  incompletely  excised  the 
recurrence  rate  exceeded  70%.^  Any  residual  lym- 
phangioma is  susceptible  to  infection  and  recurrence. 
The  unroofing  of  residual  cysts  may  potentiate  the 
cure.  These  patients  must  have  vigorous  preoperative 
treatment  of  oral  infection  and  preparation  of  the  skin. 
Antibiotics  should  be  used  when  infection  is  present 
and  prophy tactically  during  the  perioperative  period. 
Surgical  drains  and  pressure  dressing  should  be  used 
to  eliminate  potential  spaces.  Surgical  complications 
have  included  muscle  weakness,  Horner's  syndrome, 
recurrent  laryngeal  nerve  paralysis,  post-operative  in- 
fection, recurrence,  airway  obstruction,  and  death. 

CASE  STUDY 

An  11-day-old  black  female  was  noted  to  have  a small 
sublingual  lesion  on  incidental  exam.  Four  months 
later,  she  developed  a tender  enlarging  submaxillary 
mass,  which  was  fluctuant  and  erythematous,  and 
she  was  treated  with  parenteral  antibiotics  and  hos- 
pitalization. Eventually  she  was  referred  to  the  Tulane 
Department  of  Otolaryngology  with  the  diagnosis  of 
lymphangioma.  She  then  developed  inspiratory  stri- 
dor and  dysphagia.  At  six  months  of  age  she  was 
taken  to  surgery  for  excision  of  this  enlarging  mass. 
Treatment  required  tracheotomy  and  bilateral  modi- 
fied radical  neck  and  supramyelohyoid  dissections. 
Some  residual  tumor  remained  within  the  lingual 
musculature.  At  both  two  months  and  one  year  later 
she  required  laser  excision  of  hypopharyngeal  lym- 
phangioma. She  is  now  being  followed  in  our  clinic 
with  recurrent  tumor  in  the  hypopharynx,  tongue, 
and  lower  one-third  of  the  face,  and  she  will  require 
reexcision  and  repeat  laryngoscopy. 

CONCLUSION 

Lymphangioma  is  a benign  congenital  lymphatic  mal- 
formation which  presents  difficult  management  de- 
cisions. In  a most  serious  situation,  lymphangioma  in 
the  neck  can  cause  life  threatening  airway  compro- 
mise and  deglutition  difficulty  and  must  be  treated 
with  urgency.  Radical  surgery  preserving  function  and 
anatomic  structure  has  been  the  treatment  of  choice 
in  most  patients.  ■ 


REFERENCES 

1.  Saigo  M,  Munro  IR,  Mancer  K:  Lymphangioma:  A long  term  followup 
study.  Blast  Reconstr  Surg  1975;56:642-651. 

2.  Wemher  A:  Die  Angeborenen  Zysten-Hygrome  und  die  inhen  verwandten 
Geschwulste  in  anatomisher  diagnostischer  und  thrapeutischer  Beziehung.  Gies- 
sen, GF  Heyer,  1843:p76. 

3.  Dowd  CN:  Hygroma  cysticum  coUi:  Its  structure  and  etiology.  Ann  Surg 
1913;58:112-132. 

4.  Landing  BH,  Farber  S:  Atlas  of  Tumor  Pathology.  Washington,  DC,  Armed 
Forces  Institute  of  Pathology,  1956,  Sec  III,  fasc  7. 

5.  Cohen  S,  Thompson  J:  A survey  of  pediatric  lymphangioma.  Ann  Otol 
Rhinol  Laryngol  [Suppl]  1987;l-20. 

6.  Briggs  D,  Leix  F,  Snyder  WH,  et  al:  Cystic  and  cavernous  lymphangioma. 
West } Surg  1953;61:499-506. 


Drs  Mentz,  Graham,  and  Blair  are  from  the  Dept  of  Otolaryngology- 
Head  & Neck  Surgery  at  Tulane  Medical  School  in  New  Orleans. 

Reprint  requests  should  be  sent  to  Paul  A.  Blair,  MD,  Dept  of 
Otolaryngology-Head  & Neck  Surgery,  Tulane  Medical  School,  1430 
Tulane  Ave,  New  Orleans,  LA  70112. 


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JOURNAL  VOL  140  MARCH  15 


FEEDING  PRACTICES  OF 
LOW-INCOME  INFANTS: 

A NEW  ORLEANS  HEALTH  DEPARTMENT  STUDY 


HOSEA  J.  DOUCET,  MD,  MPH;  ROY  A.  BERRY 


16  JOURNAL  VOL  140  MARCH 


A survey  of  infants  from  birth  to  1 year  of  age  was 
conducted  at  city-operated  Child  Health  Centers  to 
determine  the  infant  feeding  practices  and 
attitudes  toward  nutrition  of  needy  participants  of 
federal  nutrition  programs.  It  was  determined  that 
in  this  largely  black  population,  88%  of  the  infants 
were  bottle-fed,  27%  had  cereal  introduced  by  age 
1 month,  and  many  were  already  on  cola  drinks. 
Most  participants  recalled  receiving  information  on 
breast-  or  bottle-feeding  but  few  recalled  receiving 
information  on  the  introduction  of  foods  other 
than  milk.  Most  parents  (76%)  desired  more 
information  on  the  subject.  Participants  in  these 
programs  were  clearly  not  practicing  the  current 
recommended  guidelines  on  infant  nutrition  with 
regard  to  introduction  of  foods  other  than  milk. 
The  nutrition  education  efforts  in  public  health 
clinics  should  emphasize  more  teaching  on  the 
appropriate  timing  for  introduction  of  foods  other 
than  milk  into  the  diet  of  infants,  especially  since 
parents  have  expressed  an  interest  in  this  area. 

INFANT  FEEDING  PRACTICES  in  the  period  from  birth 
through  one  year  vary  greatly  among  different  pop- 
ulation groups  in  this  country  and  throughout  the 
world.  For  centuries,  human  breast  milk  was  the  only 
available  source  of  nutrition  for  infants  during  the  first 
few  months  of  life.  Since  the  introduction  of  com- 
mercial infant  formulas  in  the  30s  and  40s,  breast- 
feeding has  declined  in  the  United  States  reaching  a 
low  point  of  22%  to  25%  in  the  early  70s.^  Breast- 
feeding then  began  an  upward  trend  which  has  con- 
tinued until  the  present.  The  national  incidence  of 
infants  breast-feeding  in  the  hospital  was  reported  to 
be  as  high  as  58%  in  1981.^  The  rate  of  increase  of 
breast-feeding  has  been  slower  in  the  less  educated 
and  lower  socioeconomic  groups  which  continue  to 
have  relatively  low  levels  of  breast-feedings.^  Infants 
are  also  receiving  supplemental  foods  other  than  breast 
irdlk  or  formula  at  an  early  age.^  The  American  Acad- 
emy of  Pediatrics  (AAP)  and  other  professional  or- 
ganizations recommend  breast-feeding  as  almost  al- 
ways preferable  to  commercial  formulas,  and  they 
also  recommend  that  foods  other  than  breast  milk  or 
formula  not  be  introduced  prior  to  the  age  of  four  to 
six  months,  at  which  time  the  addition  of  iron  en- 
riched foods  is  encouraged.^'  ^ 

This  study  was  undertaken  to  determine  infant 


feeding  practices  and  attitudes  toward  nutrition  among 
federal  nutrition  program  participants  attending  Child 
Health  Centers  (previously  called  Well  Baby  Clinics) 
operated  by  the  New  Orleans  Health  Department. 
Determination  of  this  more  precise  information  can 
facilitate  the  nutrition  education  component  of  these 
programs. 

METHODS 

During  the  summer  of  1984,  409  adults  accompanying 
infants  from  birth  through  1 year  were  interviewed 
at  six  of  the  eight  Child  Health  Centers  operated  by 
the  New  Orleans  Health  Department.  At  these  cen- 
ters patients  receive  routine  immunizations,  physical 
examinations,  growth  and  development  determina- 
tions, and  screenings  for  anemia,  lead  poisoning,  vi- 
sion, and  hearing  problems.  In  addition  they  may  be 
eligible  to  receive  nutritional  counseling  and  certifi- 
cation in  either  of  two  federal  nutritional  programs: 
Women,  Infant  and  Children  (WIC)  or  Commodity 
Supplemental  Food  Program  (CSFP).  To  qualify  for 
these  programs,  an  infant  had  to  meet  residential  re- 
quirements (Orleans  Parish),  financial  requirements 
(145%  to  185%  of  poverty  level),  and  nutritional  cri- 
teria established  by  the  US  Department  of  Agricul- 
ture. The  CSFP  provides  monthly  food  packages  of 
infant  formula  and/or  food  supplements  to  families. 
The  WIC  Program  provides  a series  of  vouchers  which 
can  be  used  at  participating  food  stores  to  purchase 
designated  foods  and  infant  formula.  These  programs 
target  the  low  income,  high  risk  population  of  chil- 
dren from  birth  to  6 years  of  age.  Orleans  Parish  has 
a total  participation  of  approximately  4,500  infants  on 
the  WIC  program  and  22,000  infants  and  family  mem- 
bers on  the  CSFP.  This  does  not  include  participation 
in  the  Elderly  CSFP. 

During  the  interviews,  three  students  of  the  Tu- 
lane  School  of  Public  Health  and  Tropical  Medicine 
administered  a standardized  questionnaire  according 
to  set  criteria.  The  questionnaire  was  read  to  individ- 
ual adults  accompanying  infants  in  the  clinic  waiting 
rooms.  All  persons  interviewed  were  participants  in 
one  of  the  two  food  programs.  Individuals  not  par- 
ticipating in  either  program  were  excluded  from  the 
study.  The  questionnaire  was  devised  to  answer  ques- 
tions regarding  the  incidence  of  breast-and  formula- 
feeding, the  timing  of  the  introduction  of  other  foods, 

JOURNAL  VOL  140  MARCH  17 


Fig  1.  TIMING  OF  INTRODUCTION  OF  NON-MILK  FOODS  INTO  THE  DIET 
OF  INFANTS  BY  1 MONTH  AND  3 MONTHS  OF  AGE 


AGE  ONE  MONTH  I I AGE  THREE  MONTHS  [ 


food  preparation  techniques, 
and  the  sources  of  information 
upon  which  feeding  decisions 
were  based.  Each  interview 
lasted  approximately  30  min- 
utes. 

RESULTS 

The  majority  of  infants  in  this 
study  were  black  (89%)  with 
the  remainder  racially  divided 
among  Asian,  Hispanic,  and 
white  populations.  The  aver- 
age infant's  age  was  5 months 
and  the  average  maternal  age 
was  24  years.  Prenatal  care  for 
most  participants  had  been 
provided  by  Charity  Hospital 
of  New  Orleans  (61%).  No  sig- 
nificant differences  in  the  re- 
sults from  the  six  different  clinic 
sites  were  noted. 

The  most  common  method 
of  infant  feeding  was  deter- 
mined to  be  bottle-feeding 
(88%).  Only  7%  of  infants  were 
breast-fed  exclusively,  and  5%  of  infants  were  both 
breast-and  bottle-fed.  Among  the  bottle-feeders,  58% 
considered  breast-feeding  or  a combination  of  breast- 
and  bottle-feeding  to  be  healthier  than  bottle-feeding 
only.  Most  attendants  stated  that  they  chose  bottle- 
feeding  because  it  was  "easier"  (41%)  or  stated  that 
they  had  never  considered  breast-feeding  (31%);  only 
7%  gave  medical  reasons  or  a physician's  recommen- 
dation as  the  reason  for  choosing  that  method.  Of  the 
participants  currently  bottle-feeding,  only  20%  had 
previously  breast-fed  the  child  they  accompanied  to 
the  clinic  or  had  breast-fed  an  earlier  child;  80%  had 
never  attempted  breast-feeding. 

Participants  were  asked  when  supplemental  foods 
other  than  milk  or  formula  were  first  introduced  into 
their  infants'  diet.  Many  had  already  done  so  by  age 
1 month  (Fig  1).  A total  of  27%  of  these  infants  had 
cereal  introduced  by  the  age  of  1 month  or  earlier. 
Several  infants  had  foods  other  than  milk  introduced 
during  the  first  week  of  life.  By  the  age  of  3 months, 
54%  of  the  409  infants  had  been  introduced  to  cereal. 


39%  had  received  fruits  or  fruit  juices,  24%  had  re- 
ceived vegetables,  and  9%  had  received  meats.  Many 
participants  were  currently  giving  cola  drinks  (17%) 
or  Kool-Aid®  mixtures  (18%)  to  their  infants.  Of  the 
participants,  33%  admitted  to  regularly  adding  sugar 
or  syrup  to  their  infants'  drinking  water. 

The  majority  of  participants  indicated  that  infor- 
mation on  infant  feeding  had  been  provided  by  a 
physician  or  a nurse  (Table  1).  However,  more  of 
these  participants  remembered  receiving  information 
on  breast-and  bottle-feeding  than  remembered  re- 
ceiving information  on  the  introduction  of  other  sup- 
plemental foods.  A total  of  35%  stated  that  they  re- 
ceived no  information  on  the  introduction  of  foods 
other  than  milk.  A smaller  number  stated  that  they 
had  received  no  information  on  breast-  (19%)  or  bot- 
tle-feeding (21%).  A total  of  76%  wanted  more  infor- 
mation on  the  introduction  of  supplemental  foods; 
54%  wanted  more  information  on  bottle-feeding;  only 
38%  stated  that  they  wanted  additional  information 
on  breast-feeding. 


18  JOURNAL  VOL  140  MARCH 


DISCUSSION 


Prior  to  this  century,  the  most  important  food  avail- 
able to  an  infant  during  the  first  months  of  life  was 
human  breast  milk.  During  these  first  few  months, 
cow's  milk,  which  has  a high  osmolarity  and  an  excess 
renal  excretory  load  of  protein  and  minerals,  is  poorly 
tolerated  by  human  infants.  An  infant  could  not  in- 
gest "adult"  or  solid  foods  until  about  the  age  of  six 
months  when  he  could  chew,  swallow,  and  exhibit 
good  head  control.  Therefore,  it  was  several  months 
before  other  foods  could  be  added  to  his  diet. 

Today,  however,  a wide  variety  of  food  is  avail- 
able to  an  infant  during  his  first  year.  Most  commer- 
cial formulas  are  modified  from  a cow's  milk  base  with 
levels  of  protein  and  ash  decreased  to  levels  near  those 
of  human  milk.^  Other  milks  or  milk  substitutes  are 
available  for  infants  who  cannot  tolerate  cow's  milk, 
and  as  more  is  learned  about  infant  physiology,  prep- 
arations are  improved  accordingly.  With  current 
methods  of  grinding,  straining,  and  preserving,  foods 
which  were  once  only  "adult"  foods  are  now  available 
as  baby  foods,  eg,  spinach,  turkey,  beef.  These  baby 
foods  can  be  ingested  at  very  early  ages,  even  during 
the  first  weeks  of  life. 

These  changes  are  not  without  consequences, 
however,  and  do  not  mean  that  cow's  milk  and  other 
foods  are  satisfactory  replacements  for  the  once  tra- 
ditional mainstay  of  mankind  — human  breast  milk. 
The  AAP  has  recommended  that  "breast  milk  is  al- 
most always  preferred  to  formula."^  Reasons  often 
cited  include  the  association  of  breast-feeding  with 
fewer  infections,  fewer  allergic  problems,  optimum 
nutrition  during  growth,  and  improved  psychological 
and  intelligence  levels.^ 

Based  on  this  study,  it  appears  that  current  rec- 
ommendations on  infant  feeding  practices  during  the 
first  year  of  life  are  not  being  adequately  followed  in 
our  population.  Most  mothers  in  this  study  were  not 
breast-feeding,  although  most  of  those  interviewed 
felt  that  breast-feeding  would  be  better  for  their  in- 
fant. Unfortunately,  they  had  decided  to  bottle-feed 
in  spite  of  this.  Furthermore,  60%  did  not  desire  any 
more  information  on  the  subject  of  breast-feeding. 

Other  studies  have  stated  multiple  reasons  why 
mothers  do  not  breast-feed.^  Many  mothers  consider 
breast-feeding  inconvenient  for  a modern  lifestyle, 
find  it  embarrassing,  or  have  a fear  of  inadequate 


TABLE  1 

SOURCES  OF  INFORMATION  ON  INFANT  FEEDING 


Source  Breast  Bottle  Other  Foods 


Physician 

26% 

24% 

16% 

Nurse 

60% 

60% 

37% 

Friend 

3% 

6% 

4% 

Relative 

3% 

7% 

8% 

No  one 

19% 

21% 

35% 

Others 

6% 

6% 

9% 

lactation,  infection,  or  cosmetic  after-effects  of  breast- 
feeding. The  knowledge  of  breast-feeding  that  was 
traditionally  passed  from  mother  to  daughter  has  also 
largely  been  lost. 

It  has  been  reported  by  other  investigators  that 
the  decision  on  the  method  of  feeding  was  made  be- 
fore pregnancy  by  60%  of  mothers  who  breast-fed  and 
40%  of  mothers  who  bottle-fed.^  Very  few  mothers  in 
this  study  reported  waiting  until  after  delivery  to  de- 
cide to  breast-feed  (10%)  or  bottle-feed  (20%).  This  is 
confirmed  in  our  study  by  the  small  number  of  our 
participants  requesting  more  information  on  breast- 
or  bottle-feeding  at  the  time  of  their  visits  to  the  Child 
Health  Centers.  Due  to  the  large  majority  of  mothers 
bottle-feeding  today,  there  is  little  incentive  for  a 
mother  to  make  the  decision  to  breast-feed  at  the  time 
of  delivery.  There  is  even  less  incentive  for  a low- 
income  mother  to  decide  to  change  feeding  methods 
once  she  attends  a well  baby  clinic,  and  bottle-feeding 
has  become  well  established.  Therefore,  a more  ef- 
fective time  to  promote  breast-feeding  is  prior  to  an 
infant's  delivery.  In  this  manner,  mothers  can  ade- 
quately prepare  for  breast-feeding  and  the  misinfor- 
mation previously  stated  can  be  corrected.  As  noted, 
most  mothers  attending  the  Child  Health  Centers  were 
not  interested  in  further  information  on  breast-feed- 
ing or  bottle-feeding. 

Concerning  the  introduction  of  supplemental 
foods,  the  majority  of  infants  in  this  study  had  foods 
other  than  milk  introduced  by  the  age  of  3 months, 
and  over  one  quarter  had  started  cereal  by  the  age  of 
1 month.  While  these  figures  were  not  quantified,  and 
we  cannot  assess  their  fuU  impact,  this  information 

JOURNAL  VOL  140  MARCH  19 


indicates  serious  variations  from  professional  rec- 
ommendations. The  participants  of  this  study  appar- 
ently recognized  their  ignorance  on  when  to  intro- 
duce foods  other  than  milk,  and  over  three  fourths 
wanted  more  information  on  this  subject. 

Reasons  often  cited  for  the  early  introduction  of 
supplemental  foods  include  a desire  of  mothers  to  see 
their  infants  gain  weight  rapidly,  social  pressure  to 
conform  to  how  other  (often  older)  children  were  fed, 
effective  marketing  by  the  infant  food  industry,  and 
the  belief  that  the  feeding  of  solid  food  will  help  an 
infant  to  sleep.  None  of  these  reasons  has  any  nutri- 
tional advantage,  and  each  should  be  countered  in 
any  educational  program.  The  early  introduction  of 
supplemental  foods  can  have  widespread  and  pos- 
sibly harmful  effects  which  include  development  of 
diarrhea,  food  and/or  other  allergies,  obesity,  and  poor 
nutritional  habits.® 

Prior  to  the  age  of  4 to  6 months,  an  infant  lacks 
the  neuromuscular  control  of  the  head  and  neck  nec- 
essary for  chewing  and  swallowing  foods  as  well  as 
the  ability  to  indicate  a desire  for  more  or  less  food. 
Also,  in  the  first  few  months  of  life,  the  intestinal  tract 
and  kidneys  have  not  developed  the  proper  mech- 
anisms for  coping  with  foreign  proteins  and  electro- 
lytes, but  are  designed  to  digest  the  proteins,  lipids, 
and  carbohydrates  found  in  breast  milk.  The  AAP 
recommends  that: 

At  about  four  to  six  months  of  age,  a variety 
of  foods  should  be  introduced  one  at  a time,  at 
intervals  of  a week  or  more.  The  sequence  of 
foods  is  not  critical,  but  iron-fortified,  single- 
grain infant  cereals  are  a good  early  choice.  The 
addition  of  individual  (not  mixed)  vegetables, 
fruits,  or  meats  introduces  a variety  of  foods  and 
sets  the  pattern  for  a diversified  diet.^ 


and  many  of  these  infants  were  currently  on  cola  or 
Kool-Aid®  drinks.  There  is  an  equal  need  for  educa- 
tion on  breast-feeding  in  this  population,  but  the  most 
appropriate  and  most  effective  time  for  this  education 
is  prior  to  attendance  at  well  baby  clinics.  ■ 

REFERENCES 

1.  Hendershot  GE:  Domestic  review,  trends  in  breast-feeding.  Pediatrics 
1984;74(supp):591-602. 

2.  American  Academy  of  Pediatrics:  On  the  Feeding  of  Supplemental  Foods 
to  Infants.  Pediatrics  1980;65:1178-1181. 

3.  Foman  SJ:  What  are  infants  fed  in  the  United  States?  Pediatrics  1975;56:350- 
354. 

4.  American  Academy  of  Pediatrics:  Breast-feeding.  Pediatrics  1978;62:591- 
601. 

5.  Miller  SA,  Chopra  JG:  Problems  with  human  milk  and  infant  formulas. 
Pediatrics  1984;74(supp):639-647. 

6.  Simopoulos  AP,  Grave  GD:  Factors  associated  with  the  choice  and  du- 
ration of  infant-feeding  practice.  Pediatrics  1984;74(supp):603-614. 

7.  Sacks  SH,  Brada  M,  Hill  AM,  et  al:  To  breast  feed  or  not  to  breast  feed. 
Practitioner  1965;216:183-191. 

8.  Leberthal  E:  Impact  of  digestion  and  absorption  in  the  weaning  period 
on  infant  feeding  pracHces.  Pediatrics  1985;75(supp):207-215. 


Dr  Doucet  is  the  Chief  of  Clinical  Services/Communicable  Diseases  of 
the  New  Orleans  Health  Department  and  Associate  Professor  of 
Pediatrics  at  Tulane  University  School  of  Medicine  in  New  Orleans. 

Mr  Berry  was  a senior  medical  student  at  Tulane  University  School  of 
Medicine  and  a candidate  for  the  combined  MD/MPH  degree.  He  has 
since  graduated  and  is  currently  an  intern  in  internal  medicine  at  the 
University  of  California  at  Davis  in  Sacramento,  California. 

Reprint  requests  should  be  sent  to  Hosea  }.  Doucet,  MD,  MPH, 
Associate  Professor  of  Pediatrics,  Tulane  University  School  of  Medicine, 
Dept  of  Pediatrics,  1430  Tulane  Ave,  New  Orleans,  LA  70112. 


CONCLUSION 

In  this  population  of  low-income  mothers  and  infants, 
there  is  apparently  a great  need  and  desire  for  edu- 
cation on  how  to  introduce  foods  other  than  breast 
milk  or  formula.  Participants  in  this  study  were  in- 
troducing supplemental  foods  at  too  early  an  age  but 
were  desirous  of  more  information.  Over  one  fourth 
of  the  infants  had  cereal  introduced  before  1 month 
of  age,  over  one  half  had  cereal  added  before  3 months. 


20  JOURNAL  VOL  140  MARCH 


TREATMENT  OF  IMPOTENCE 

NONSURGICAL  MODALITIES 


NEIL  H.  BAUM,  MD 


Impotence  may  result  from  a primary  disorder  of 
the  male  reproductive  system  or,  more  commonly, 
from  physical  or  psychogenic  disturbances.  Recent 
advances  in  the  pathophysiology  of  the  erection 
mechanism  has  led  to  the  development  of 
nonsurgical  treatment  of  this  common  sexual 
dysfunction.  This  is  the  first  of  a two-part  series. 
A future  article  discusses  the  surgical  approach  to 

impotence. 


Men  have  historically  looked  for  the  pill,  injec- 
tion, or  magic  potion  that  could  restore  their 
youth  and  potency  without  surgery  and  without  side 
effects.  Unfortunately,  the  ideal  nonsurgical  treat- 
ment has  not  been  discovered.  However,  great  ad- 
vances in  this  common  medical  problem  that  affects 
nearly  10  million  American  men  have  taken  place  in 
the  last  few  years.  This  paper  will  review  some  of  the 
latest  nonsurgical  treatments. 

NO  TREATMENT 

It  is  not  unusual  for  a man  to  learn  that  his  erectile 
failure  is  on  a physical  basis  and  accept  the  diagnosis 
without  any  further  workup  or  treatment.  Often- 
times, the  partner  of  an  impotent  man  has  a conscious 
or  subconscious  question  of  infidelity.  In  this  situa- 
tion, the  man  wants  to  convince  his  partner  that  there 
is  no  loss  of  love  or  affection  and  that  no  third  party 
is  involved.  If  the  physician  recognizes  this  set  of 
circumstances,  he  can  be  very  helpful  in  alleviating  a 
great  source  of  anxiety  and  tension  by  reassuring  the 
man's  partner  that  the  impotence  is  on  an  organic  or 
physical  basis  and  that  there  is  no  loss  of  love  or 
affection.  ^ 


JOURNAL  VOL  140  MARCH  27 


HORMONE  REPLACEMENT 


PROLACTIN 


The  subject  of  androgen  replacement  for  erectile  dys- 
function is  an  area  of  considerable  controversy.  It  is 
well  documented  that  the  serum  testosterone  level 
declines  only  minimally  with  age.  The  total  serum 
testosterone  level  usually  remains  within  a normal 
range  until  age  70.  Several  studies  have  shown  that 
the  serum  testosterone  level  is  not  lower  in  impotent 
men  than  in  potent  men.^'^  It  is  also  well  accepted 
that  serum  testosterone  is  more  responsible  for  main- 
taining the  libido  or  sex  drive  than  for  obtaining  or 
maintaining  an  erection.  Recently  more  information 
regarding  the  pathophysiology  of  the  hypothalamic- 
pituitary-testicular  axis  has  become  available  and  more 
cases  of  endocrinologic  impotence  are  being  discov- 
ered. It  is  important  that  all  impotent  patients  have 
a screening  serum  testosterone  level.  Low-normal  or 
decreased  levels  require  a more  thorough  endocrine 
evaluation. 

Patients  with  documented  decreased  testoster- 
one levels  usually  have  an  excellent  response  to  an- 
drogen replacement.  Intramuscular  injections  of  a long 
acting  testosterone  supplement  such  as  testosterone 
enanthate  produce  a dose-related  increase  in  the  li- 
bido as  well  as  in  frequency  and  quality  of  erections. 
The  intramuscular  route  is  preferred  to  oral  admin- 
istration because  of  the  variable  absorption  from  the 
gastrointestinal  tract  and  the  association  of  cholestatic 
jaundice  with  oral  testosterone.  It  is  important  that 
aU  patients  receiving  long-term  androgen  therapy  have 
periodic  liver  function  tests.  All  patients  over  age  50 
require  frequent  rectal  examinations  and  measure- 
ments of  serum  acid  phosphatase  since  exogenous 
androgens  can  activate  a carcinoma  of  the  prostate. 
There  are  no  clear  cut  guidelines  for  the  use  of  an- 
drogens in  the  impotent  patient  with  a normal  serum 
testosterone  and  no  obvious  organic  pathology.  I think 
that  a “short  course"  of  androgen  therapy  often  is 
beneficial  and  is  associated  with  negligible  morbidity. 
The  general  improvement  in  well-being  and  sexual 
performance  is  most  likely  related  to  either  the  ana- 
bolic effects  of  the  androgen  or  the  expectation  of 
improvement  associated  with  the  physician's  confi- 
dence that  the  problem  is  amenable  to  treatment  rather 
than  to  any  specific  endocrine  action  on  potency. 


Recently  there  has  been  an  increased  awareness  of 
the  association  of  the  role  of  prolactin  and  impotence. 
One  study  reported  19%  of  impotent  patients  referred 
for  medical  evaluation  were  found  to  have  hypotha- 
lamic-pituitary disease.  Nearly  one-quarter  of  these 
patients  had  prolactin  secreting  tumors.^  Although 
this  statistic  seems  high,  it  is  important  to  rule  out 
this  treatable  cause  of  impotence.  Most  patients  with 
prolactin  secreting  tumors  are  impotent  and  in  nearly 
half  of  these  patients,  the  chief  complaint  is  impo- 
tence. Most  patients  will  have  a low-normal  or  slightly 
decreased  serum  testosterone  level.  The  diagnosis  is 
confirmed  by  elevated  levels  of  prolactin.  The  finding 
of  hyperprolactinemia  warrants  a complete  pituitary 
evaluation.  The  treatment  of  impotence  associated 
with  hyperprolactinemia  has  been  successful  with  the 
use  of  the  long-acting  dopamine  receptor  agonist 
bromocriptine  mesylate.  This  drug  decreases  the  el- 
evated prolactin  and  consequently  raises  the  testos- 
terone level  with  improvement  in  libido  and  potency. 

DRUG-ASSOCIATED  IMPOTENCE 

The  list  of  medications  associated  with  sexual  im- 
pairment is  lengthy.'^  The  most  common  categories 
include  antihypertensives,  sedatives,  tranquilizers, 
analgesics,  antiandrogens,  anticholinergics,  and  drugs 
with  abuse  potential.  I believe  patients  should  be  in- 
formed about  the  sexual  side  effects  of  these  drugs; 
however,  the  likelihood  of  this  complication  should 
be  minimized,  otherwise  patients  can  conveniently 
"develop"  impotence  as  a result  of  the  self-fulfilling 
prophecy  generated  by  a well-meaning  physician.  It 
is  also  important  to  stress  to  the  patient  that  if  a sexual 
dysfunction  occurs,  they  should  report  the  problem 
rather  than  discontinue  the  medication.  Oftentimes 
the  sexual  side  effects  of  medication  can  be  reversed 
by  decreasing  the  dose  or  changing  to  another  class 
of  drug  that  accomplishes  the  same  goal  but  without 
producing  erectile  dysfunction. 

INTRACORPORAL  INJECTION 

Self-injection  of  vasodilating  drugs  into  the  penis  has 
been  a new  nonsurgical  modality  for  treating  organic 
impotence.  Several  drugs  have  been  tried  but  the  most 
successful  is  a combination  of  papaverine  hydrochlo- 


28  JOURNAL  VOL  140  MARCH 


ride  and  phentolamine  mesylate.^  This  has  been  an 
effective  treatment  regardless  of  the  age  of  the  patient 
or  the  etiology  of  the  erectile  dysfunction.  The  patient 
usually  obtains  an  erection  in  five  to  ten  minutes  after 
injection  into  one  of  the  corporal  bodies  of  the  penis. 
The  erection  usually  lasts  30  to  45  minutes.  Compli- 
cations are  rare  and  consist  of  ecchymosis  at  the  in- 
jection site,  corporal  fibrosis  if  the  same  injection  site 
is  used  repeatedly,  and  prolonged  erection  which  can 
be  reversed  by  aspiration/irrigation  with  epineph- 
rine.^ I recommend  that  patients  do  not  use  intracor- 
poral injections  more  frequently  than  once  a week. 
The  Food  and  Drug  Administration  has  not  approved 
or  disapproved  the  use  of  papaverine  hydrochloride/ 
phentolamine  mesylate  for  intracorporal  injections. 
Consequently,  I request  that  the  patients  sign  a spe- 
cial informed  consent  form  and  that  they  watch  a 
video  tape  on  sterile  technique.  The  use  of  intracor- 
poral injections  has  been  an  accepted  modality  for 
many  patients  with  organic  impotence  who  do  not 
wish  to  have  surgery  or  who  cannot  afford  surgery. 

ALPHA-ADRENERGIC  ANTAGONIST 

Recently  the  role  of  catecholamines  and  their  con- 
tribution to  the  physiology  of  erections  has  been  de- 
scribed. Yohimbine  is  an  alpha  adrenergic  blocking 
agent  derived  from  the  bark  of  an  African  tree.  This 
drug  has  been  demonstrated  to  be  successful  in  the 
management  of  “selected  cases"  of  organic  impo- 
tence.^ The  drug  is  well  tolerated  with  only  occasional 
nausea  and  dizziness  that  subsides  when  the  dosage 
is  decreased  and  then  increased  by  small  increments. 

GADGETS 

There  are  a number  of  devices  that  patients  can  pur- 
chase over-the-counter  that  can  "create  an  erection." 
Most  of  these  devices  work  on  the  principle  of  placing 
a stiff  silicone  condom  over  the  penis  then  applying 
negative  pressure  to  increase  the  blood  supply  into 
the  vascular  chambers  of  the  penis.  With  an  increase 
in  the  blood  supply  the  penis  becomes  rigid  and  a 
rubber  band  or  tourniquet  is  applied  at  the  base  of 
the  penis  to  trap  the  blood  within  the  penis.  These 
devices  are  somewhat  cumbersome  to  use  and  their 
use  can  be  complicated  by  ecchymoses  and  priapism 
if  the  tourniquet  is  left  in  place  too  long. 


SEX  THERAPY 

The  most  successful  treatment  of  psychogenic  im- 
potence is  sex  therapy.  It  is  important  that  the  patient 
and  his  partner  be  referred  to  a qualified  sex  therapist, 
a psychologist,  or  a psychiatrist  who  has  an  interest 
and  expertise  in  the  management  of  sexual  dysfunc- 
tions. The  highest  success  rate  in  the  treatment  of 
impotence  by  sex  therapy  is  in  the  patient  who:  1) 
has  had  impotence  less  than  one  year,  2)  has  a stable 
relationship  with  his  partner,  3)  has  motivation  to 
enter  sex  therapy,  and  4)  has  a partner  willing  to 
participate  with  him  in  treatment. 

SUMMARY 

Male  sexual  dysfunction  is  a concern  that  is  quite 
prevalent  in  our  society.  Until  recently  the  only  treat- 
ment for  impotence  was  sex  therapy  and  penile 
prostheses.  Now,  with  greater  understanding  of  the 
pathophysiology  of  the  erection  mechanism,  effective 
new  nonsurgical  treatment  is  available.  ■ 

REFERENCES 

1.  Federman  DD:  The  assessment  of  organic  function:  The  testis.  N Engl  J 
Med  1971;285:901. 

2.  Smith  KD:  Rapid  oscillations  in  plasma  levels  of  testosterone,  lutenizing 
hormone,  and  follicle-stimulating  hormone  in  men.  Fertil  Steril  1974;25:965. 

3.  Spark  RF:  Neuroendocrinology  and  impotence.  Ann  Intern  Med  1983;98:103. 

4.  Van  Arsdalen  K,  Wein  A:  Drug-induced  sexual  dysfunction  in  older  men. 
Geriatrics  1984;39:63. 

5.  Zorgniotti  A,  Lefleur  R:  Autoinjection  of  the  corpus  cavemosum  with  a 
vasoactive  drug  combination  for  vasculogenic  impotence.  / Urol  1985;133:39- 
41. 

6.  Padma-Nathan  H,  Goldstein  1,  Krane  R:  Treatment  of  prolonged  or  pria- 
pistic  erections  following  intracavernosal  papaverine  therapy.  Semin  Urol 
1986;4:236-238. 

7.  Morales  A,  Surridge  HC,  Marshall  PG,  et  al:  Nonhormonal  pharmacol- 
ogical treatment  of  organic  impotence.  / Urol  1982;128:45-47. 


Dr  Baum  is  a urologist  affiliated  with  Touro  Infirmary  in 

New  Orleans. 

Reprint  requests  should  be  sent  to  Dr  Baum  at  3525  Prytania  St, 
Suite  614,  New  Orleans,  LA  70115. 


JOURNAL  VOL  140  MARCH  29 


PHYSICIANS^ 
SCHEDULE 
SOME  TIME  FOR 
YOUR  COUNTRY. 

Many  physicians  would 
like  to  devote  some  time  to  their 
country  in  a local  Army  Reserve 
unit.  We  know  that  making  a 
weekend  commitment  can  be 
difficult  for  most  physicians.  So  it 
is  practical  for  the  Army  Reserve 
units  to  be  flexible  about  time. 
It’s  worth  discussing. 

Incidentally,  in  addition 
to  satisfying  your  own  desire  to 
serve  your  country,  there  are 
exceptional  opportunities  to  do 
something  totally  different  from 
a day-to-day  routine.  Oppor- 
tunities to  study  new  areas  of 
medicine,  meet  new  people  in 
your  specialty,  and  be  a part  of 
one  of  the  world’s  most  advanced 
medical  teams. 

Discuss  the  opportunities 
with  our  Army  Medical  Person- 
nel Counselor. 


FOR 

SURGEONS 
LOOKING  FOR 
ACHAUENGE. 

Your  challenge  could  be  the 
Army  Reserve  unit  near  you.  It's  a 
unit  that  requires  the  services  of 
surgeons. 

You  may  wish  to  explore  the 
challenge  of  teaching  in  a major 
medical  center.  You  may  wish  to 
explore  the  special  challenges  of  your 
specialty  in  triage.  Certainly  you’ll  be 
confronted  by  challenges  very 
different  from  your  daily  routine. 

You’ll  also  have  an  opportunity 
to  participate  in  a number  of  pro- 
grams in  which  you’ll  be  able  to 
exchange  views  and  information  with 
other  surgeons  from  all  over  the 
country. 

The  Army  Reserve  understands 
the  time  demands  on  a busy  physi- 
cian, so  you  can  count  on  us  to  be 
totally  flexible  in  making  time  for  you 
to  share  your  specialty  with  your 
country.  We’ll  arrange  your  training 
program  to  work  with  your  practice. 

To  find  out  about  the  benefits  of 
serving  with  a nearby  Army  Reserve 
unit,  we  recommend  you  call  our 
Army  Medical  Personnel  Counselor. 


PHYSICIANS.THERE 
ARE  TWO  KINDS 
OF  FLEXIBILITY  IN 
THE  ARMY  RESERVE 
WE  THINK  YOU'LL  LIKE. 

One,  time.  We  know  how 
tough  it  is  for  a busy  physician 
to  make  weekend  time  commit- 
ments. So  we  offer  flexible 
training  programs  that  allow  a 
physician  to  share  some  time 
with  his  or  her  country.  We 
arrange  a schedule  to  suit  your 
requirements. 

Tw,  the  opportunity  to 
explore  other  phases  of  medi- 
cine, to  add  a different  kind  of 
knowledge— the  challenge  of 
military  health  care.  It’s  a flexi- 
bility which  could  prove  to  be 
both  stimulating  and  reward- 
ing, with  the  opportunity  to 
participate  in  a variety  of 
programs  that  can  put  you  in 
contact  with  medical  leaders 
from  all  over  the  country. 

See  how  flexible  we  can 
be,  call  our  Army  Medical 
Personnel  Counselor. 


ARMY  RESERVE. 
BEALLYOUCANBE. 


HERE'S  ONE  DOCTOR 
WHO  WON'T  PAY 
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New  Orleans,  LA  701 12 
Call  collect;  (504)  589-2373 


EVALUATION  OF  EXTRAVASATION 
DURING  INTRAVENOUS  UROGRAPHY 


NICHOLAS  J.  PERSICH;  EDWARD  I.  BLUTH,  MD 


Extravasation  during  intravenous  pyelography  can 
be  an  ominous  sign  indicating  frank  pelvic  or 
ureteral  rupture;  however,  it  can  also  indicate  a 
forniceal  tear  which  is  a benign  complication.  The 
authors  present  a case  and  discuss  the 
differentiation  between  true  rupture  of  the  upper 
collecting  system  and  forniceal  extravasation  in  an 

obstructed  system. 


IN  A PATIENT  who  complained  of  left  flank  pain,  in- 
travenous pyelography  with  abdominal  compres- 
sion showed  extravasation  of  contrast  from  the  left 
kidney  into  the  retroperitoneal  space.  Extravasation 
of  urine  usually  occurs  from  rupture  of  a calyceal  for- 
nix as  a result  of  obstruction.  The  primary  cause  ap- 
pears to  be  a rapid  rise  in  intrapelvic  pressure  with 
rupture  of  the  fornix  acting  as  a physiologic  release 
mechanism  to  decrease  the  intrapelvic  pressure.  This 
process  is  usually  benign  but  must  be  differentiated 
from  frank  pelvic  or  ureteral  rupture  which  requires 
surgical  intervention. 

CASE  REPORT 

A 32-year-old  man  was  seen  in  the  emergency  room 
with  left  flank  pain.  Physical  examination  revealed 
left  costovertebral  angle  tenderness  and  hematuria. 

An  intravenous  pyelogram  with  compression  was 
performed.  Scout  films  revealed  several  calcific  dens- 
ities in  the  left  kidney  and  a 5 mm  calculus  superior 
to  the  left  L-3  transverse  process  and  lying  in  the 
apparent  pathway  of  the  left  ureter.  Following  injec- 
tion of  contrast  media,  there  was  delayed  excretion  ► 

JOURNAL  VOL  140  MARCH  35 


1 


Fig  1.  90-minute  deiayed  iVP  film  demonstrating 
left  hydronephrosis.  In  addition,  consider- 
able extravasation  of  contrast  is  seen  sur- 
rounding the  pelvocalyceai  system  and 
proximal  left  ureter. 


from  the  left  kidney  with  dilatation  of  the  upper  col- 
lecting system.  Slight  extravasation  from  the  renal 
sinus  and  hilum  of  the  left  kidney  was  noted  on  the 
10-minute  film  with  subsequent  extension  down  the 
lateral  border  of  the  psoas  muscle.  Further  extrava- 
sation was  noted  on  the  90-minute  film  (Fig  1).  Con- 
trast media  had  flowed  down  the  fascial  planes  around 
the  left  ureter.  Two  days  following  the  examination, 
the  patient  underwent  extracorporeal  shock  wave 
lithotripsy  after  the  ureteral  stone  was  displaced  into 
the  kidney.  The  renal  calculus  was  fragmented  and 
all  the  stone  fragments  passed  easily.  The  patient  left 
the  hospital  the  next  day  without  evidence  of  left  renal 
calculi. 

36  JOURNAL  VOL  140  MARCH 


DISCUSSION 

In  evaluating  extravasation  during  intravenous  urog- 
raphy, it  is  important  to  determine  the  site  of  leakage 
of  the  contrast  media.  There  has  been  some  confusion 
in  the  past  as  to  the  distinction  between  a true  rupture 
of  the  upper  collecting  system  and  forniceal  extra- 
vasation in  an  obstructed  system.  In  a previously  un- 
damaged collecting  system,  when  there  is  an  increase 
in  intraluminal  pressure,  especially  if  it  is  acute,  the 
point  of  extravasation  is  at  the  weakest  point  in  the 
system  — the  calyceal  fornix.^  The  elevated  pressure 
in  obstruction  can  cause  a minute  forniceal  tear  with 
urine  or  contrast  media  leaking  into  the  renal  sinus 
and  then  dissecting  down  around  the  ureter.  The  for- 
niceal site  of  extravasation  is  felt  to  be  a normal  safety 
valve  for  alleviation  of  increased  pressure.^  This  phys- 
iologic decompression  of  the  acutely  obstructed  sys- 
tem is  not  uncommon.^  How  often  forniceal  extra- 
vasation does  occur  in  urography  depends  usually  on 
three  factors  — the  amount  of  contrast  medium  used, 
whether  abdominal  compression  is  applied,  and  the 
degree  of  obstruction.  The  incidence  of  extravasation 
was  shown  to  increase  as  the  bolus  of  contrast  that 
was  used  was  increased,  when  abdominal  compres- 
sion was  used,  and  when  the  collecting  system  was 
completely  obstructed.^  Patients  rarely  become  symp- 
tomatic from  forniceal  extravasation.  When  symp- 
toms do  occur,  they  are  usually  the  result  of  leakage 
of  infected  urine  and  formation  of  an  abscess.^ 

In  contrast  to  forniceal  extravasation,  true  rup- 
ture of  the  renal  pelvis  or  ureter  is  totally  non- 
physiologic.  Trauma  is  the  most  common  cause  with 
calculus  disease  the  next  most  common.  Rupture  has 
also  been  reported  in  a previously  damaged  collecting 
system  secondary  to  previous  kidney  surgery,  recent 
instrumentation  (ureteric  catheterization  or  retro- 
grade pyelography),  infection,  or  neoplasm.^  The 
mechanism  by  which  a calculus  causes  rupture  is  either 
from  necrosis  of  the  wall  around  the  stone  or  from  a 
tear  formed  during  the  passage  of  the  stone.  When 
the  calculus  obstructs  distally  in  the  ureter,  the  ele- 
vated pressure  that  is  produced  can  cause  the  dam- 
aged wall  to  rupture  or  it  can  increase  the  size  of  the 
original  tear  with  subsequent  rupture  and  extrava- 
sation.^ Symptoms  from  frank  rupture  of  the  pelvis 
or  ureter  are  usually  severe,  and  often  medical  and 
surgical  intervention  are  indicated.  How  aggressive 


treatment  should  be  is  based  on  the  requirements 
imposed  by  the  patient's  clinical  condition,  the  per- 
sistence of  obstruction  or  extravasation,  or  the  pres- 
ence of  a complication  such  as  urinoma  or  abscess.® 
Further  differentiation  between  these  two  entities 
may  be  aided  by  certain  observations  of  the  roent- 
genogram. The  first  is  to  look  specifically  for  contrast 
material  around  a calyx,  the  presence  of  which  clearly 
points  to  forniceal  rupture.  Secondly,  demonstration 
of  the  ureter  seems  to  be  a helpful  point  in  differ- 
entiation. In  cases  showing  tears  or  rupture  of  the 
pelvis,  the  ureter  on  the  affected  side  was  never  or 
only  occasionally  visualized,  while  in  cases  with  for- 
niceal extravasation  a typical  "pipe"  ureter  was  pres- 
ent. And  further,  re-examination  24  to  48  hours  after 
the  initial  examination  will  show,  in  most  cases  of 
forniceal  rupture,  disappearance  of  the  extravasation, 
whereas  in  cases  of  pelvic  or  ureteral  rupture,  the 
roentgenologic  appearance  remains  unchanged.  These 
conditions  are  not  without  exception.  Clinically,  also, 
there  is  a difference  between  forniceal  and  pelvic  rup- 
ture. Patients  who  experience  actual  rupture  of  the 
pelvis  or  ureter  tend  to  have  a higher  temperature, 
to  appear  more  ill,  and  to  have  an  increased  white 
blood  cell  count. ^ 

In  this  case,  the  pyelographic  appearance  and  the 
stable  clinical  condition  of  the  patient  are  consistent 
with  forniceal  rupture  as  the  cause  of  extravasation. 
Furthermore,  the  patient  had  no  past  history  of 
trauma,  instrumentation,  or  kidney  disease.  There  was 
also  no  worsening  of  symptoms  following  urography, 
making  it  unlikely  that  frank  pelvic  or  ureteral  rupture 
had  occurred.  The  importance  of  recognizing  this  type 
of  extravasation  as  a benign  complication  of  acute 
obstruction  and  distinguishing  it  from  renal  rupture 
following  trauma  cannot  be  overemphasized.  Failure 
to  understand  this  association  may  lead  to  unwar- 
ranted surgical  exploration.  ■ 

REFERENCES 

1.  Orkin  LA:  Spontaneous  nontraumatic  extravasation  from  ureter.  / Urol 
1952;67:272-283. 

2.  Khan  AU,  Malek  RS:  Spontaneous  urinary  extravasation.  / Urol  1976;116:161- 
165. 

3.  Schwartz  A,  Caine  M,  Hermann  G,  et  al:  Spontaneous  renal  extravasation 
during  intravenous  pyelography.  Am  ] Radiol  1966;98:27-39. 

4.  Bemadino  ME,  McClennan  BL:  High  dose  urography:  Incidence  and  re- 
lationship to  spontaneous  peripelvic  extravasation.  Am  J Radiol  1976;127:373- 
376. 

5.  Hadar  H,  Giro  S:  Spontaneous  extravasation  of  urine  in  chronic  ureteric 
obstruction.  Urology  1979;14:30-32. 


6.  Jeppesen  FB:  Spontaneous  rupture  of  kidney.  / Urol  1961;86:489-492. 

7.  Borkowski  A,  Canpliczka  M:  Nontraumatic  extravasation  from  the  ureter. 
Int  Urol  Nephrol  1974;5:271-275. 

8.  Abeshouse  BS:  Rupture  of  the  kidney  pelvis.  Surg  Gynecol  Obstet  1935;60:710- 
729. 

9.  Narath  PA:  Extrarenal  extravasation  obstruction  in  the  course  of  intra- 
venous pyelography.  / Urol  1978;39:65-75. 


Mr  Persich  was  a fourth  year  medical  student  at  LSU  School  of 
Medicine.  He  has  since  graduated  and  is  currently  an  intern  at  Charity 

Hospital  in  New  Orleans. 

Dr  Bluth  is  from  the  Dept  of  Radiology  at  Ochsner  Clinic  and  Alton 
Ochsner  Medical  Foundation  in  New  Orleans. 

Reprint  requests  should  be  sent  to  Dr  Bluth,  Ochsner  Clinic, 
1514  Jefferson  Hwy,  New  Orleans,  LA  70121. 


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JOURNAL  VOL  140  MARCH  37 


Physicians  Recognition  Award 

Seventeen  physicians  from  the  state  of  Louisiana  were  awarded  the  Physicians  Recognition  Award  [PRA]  during 
December,  1 987.  This  award  is  presented  by  the  American  Medical  Association  to  physicians  who  have  voluntarily 
completed  1 50  hours  of  continuing  medical  education  during  a consecutive  three-year  time  period.  Of  these  1 50 
hours,  at  least  60  must  be  in  AMA/PRA  Category  1 . These  seventeen  individuals  and  the  cities  in  which  they  reside 
are  presented  below. 


Baton  Rouge 

Francis  A.  Puyau,  MD 

Harvey 

Sof  Jan  Lamid,  MD* 

Houma 

Philip  Royce  Avet,  MD 

Jackson 

Doyne  Whittington  Loyd,  MD* 

Lafayette 

Donald  Carl  Harper,  MD 
Ricardo  Roman  Leoni,  MD 


Lake  Charles 

John  Francis  Raggio,  MD 

Monroe 

Lowery  Lee  Thompson,  MD 

New  Iberia 

George  Barry  Cousin,  MD 

New  Orleans 

Luis  Tomas  Batista,  MD* 
Edward  David  Frohlich,  MD 
Deba  Prasad  Sarma,  MD* 


Shreveport 

Horace  Edwards  Thompson,  MD 

Slidell 

Kishore  Vasudev  Kamath,  MD 

Thibodaux 

Neil  James  Maki,  MD 

Ville  Platte 

Adam  John  Tassin,  Jr.,  MD 

West  Monroe 

Gerald  Melvin  Robertson,  MD 


* These  individuals  are  not  members  of  the  Louisiana  State  Medical  Society 


New  this  year . . . 

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Special  benefit  packages  available  with  1988  membership 

A diverse  membership  has  diverse  needs,  and  the  AMA  is  committed  to  addressing 
those  needs.  This  year  we’re  introducing  something  new  when  you  join  the  AMA  or 
renew  your  membership.  In  your  AMA  Membership  Kit  you’ll  have  the  opportunity 
to  sign  up  for  one  of  three  benefit  packages  of  publications,  conferences,  participa- 
tory panels,  focused  issue  updates,  etc.,  on  topics  related  to  the  area  you  designate. 
Each  package  is  tailored  to  address  your  particular  interests: 

■ Medical  and  scientific  information  and  education  designed  to  enhance  your 
practice,  profession,  and  the  public  health. 

■ Representation  concentrated  specifically  on  economic  concerns,  such  as  professional 
liability  and  third  party  reimbursement. 

■ Representation  on  a broad  range  of  issues,  including  not  only  economic  concerns, 
but  also  quality  of  care,  ethical  issues,  public  health,  and  scientific  issues. 

To  receive  your  full  range  of  benefits,  select  one  and  only  one  of  these  free  packages 
by  filling  out  the  business  reply  card  in  your  AMA  Membership  Kit. 

Please  look  for  the  card  in  your  AMA  Membership  Kit  and  return  it  promptly.  Your 
new  benefit  package  is  one  more  way  the  AMA  supports  you  as  a pnysician. 

James  H.  Sammons,  MD 
Executive  Vice  President 


HEALTH  SCIENCn  UIHAHT 
UNIVERSITY  OP  MARYLAND 
BALTIMORE 


STACKS 


MAY  4 1988 


•IJOURNAL 

OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY  April  1988 


MOnOGlRC. 


STACKS 


Louisiana 


Physicians 


Insurance  Agency,  INC. 

A VVhollv  Owned  Subsidiary  ot  LAMMICO 


SPECIALLY  PRICED  PRODUCTS  OFFERED: 


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EDITOR 


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CHIEF  EXECUTIVE  OmCER 

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RENT  ABADIE 

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Ex  officio,  DANIEL  H.  JOHNSON  JR,  MD 

EDITORIAL  BOARD 

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WINSTON  H.  WEESE,  MD 
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PANEL  OF  CONSULTANTS 

KEN-NETH  T.  CALAMIA,  MD 
DELMAR  R.  CALDVV’ELL,  MD 
MICHAEL  E.  CAREY,  MD 
JOHN  COOKSEY,  MD 
EUGENT  J.  DABEZIES,  MD 
ROBERT  S.  DANIELS,  MD 
ADOLPH  A.  FLORES  JR,  MD 
FRAN’K  J.  ILARDI,  MD 
HENRY  W.  JOLLY  JR,  MD 
TERRY  R.  JONES,  MD 
SHELDON  P.  KOITLE,  MD 
MAXIMO  B.  LAMARCHE,  MD 
PAUL  B.  LANSING,  MD 
SAMUEL  A.  LEONARD,  MD 
BROBSON  F.  LUTZ  JR,  MD 
JOHN  c.  McDonald,  md 
PAUL  B.  MOORE,  MD 
CHARLES  B.  ODOM  JR,  MD 
JOHN  M.  RAENEY,  MD 
MARY  E.  SANDERS,  MD 
JAMES  W.  VILDIBILL  JR,  MD 
DAVID  J.  W'ERNER,  MD 


ESTABLISHED  1844.  O^smed  and  edited  by  The 
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— ■ I I ■■ 

JOURNAL 


OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY 

1988 

VOLUME  140  / NUMBER  4 / 

APRIL 

ARTICLES 

Special  issue:  Cancer  in  Louisiana 

Vivien  W.  Chen,  PhD 
Pelayo  Correa,  MD 
Jean  F.  Craig,  MS 
Elizabeth  T.H.  Fontham,  DPH 

20 

Is  cancer  survival  poorer  in 
Louisiana? 

Elizabeth  T.H.  Fontham,  DPH 
Pelayo  Correa,  MD 
Vivien  W.  Chen,  PhD 
Jean  F.  Craig,  MS 
Linda  W.  Pickle,  PhD 
Roni  Falk,  MS 

29 

Tobacco  and  cancer 

Pelayo  Correa,  MD 
Elizabeth  T.H.  Fontham,  DPH 
Vivien  W.  Chen,  PhD 
Jean  F.  Craig,  MS 
Roni  Falk,  MS 
Linda  W.  Pickle,  PhD 

43 

Diet,  nutrition,  and  cancer 

Jean  F.  Craig,  MS 
Vivien  W.  Chen,  PhD 
Pelayo  Correa,  MD 
Elizabeth  T.H.  Fontham,  DPH 

51 

Louisiana  Tumor  Registry 

Eleck  Craig,  MS 
Charles  L.  Brown  Jr,  MD 

55 

Louisiana  Cancer  and 
Lung  Trust  Fund  Board 

DEPARTMENTS 


2 

Information  for  Authors 

15 

Auxiliary  Report 

3 

New  Members 

18 

Calendar 

5 

ECG  of  the  Month 

57 

Books  Received 

11 

Otolaryngology/Head 
& Neck  Surgery  Report 

61 

Classified  Advertising 

Cover  illustration  by  Eugene  New,  New  Orleans. 


INFORMATION  FOR  AUTHORS 


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or  a statement  that  reprints  will  not  be  available. 

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essence  of  the  text  and  should  be  informative  rather  than  descriptive. 
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in  the  text.  The  following  form  should  be  followed: 

JOURNALS 

[1J  Author(s):  Use  the  surname  followed  by  initials  without  punctua- 
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used,  followed  by  "et  al."  [2]  Title  of  article.  Capitalize  only  the  first 
letter  of  the  first  word.  [3J  Name  of  journal  Followed  by  no  punctua- 
tion, underscored,  and  abbreviated  according  to  Index  Medicus.  [4] 
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use  during  surgery.  Am  I Clin  Pathol  1979;71:680-692. 

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tion. The  names  of  all  authors  should  be  given  unless  there  are  more 
than  three,  in  which  case  the  names  of  the  first  three  authors  are  used 
followed  by  "et  al."  [2]  Title,  Capitalize  the  first  and  last  word  and 
each  word  that  is  not  an  article,  preposition,  or  conjunction  of  less 
than  four  letters.  [3]  Edition  number,  [4]  Editor's  name.  [5J  Place  of 
publication,  [6]  Publisher,  [7]  Year,  [8]  Inclusive  page  numbers.  Do 
not  omit  digits. 

Example:  DeCole  EL,  Spann  E,  Hurst  RA  Jr,  et  al:  Bedside  Examina- 

tion in  Cardiovascular  Medicine,  ed  2,  Smith  JT  (ed).  New 
York,  McCraw  Hill  Co,  1986,  pp  23-37. 

ILLUSTRATIONS  should  be  submitted  in  duplicate  in  an  envelope 
(paper  clips  should  not  be  used  on  illustrations  since  the  indentation 
they  make  may  show  on  reproduction).  Legends  should  be  typed, 
double-spaced  on  a separate  sheet  of  paper.  Photographic  material 
should  be  high<ontrast  glossy  prints.  Patients  must  be  unrecognizable 
in  photographs  unless  specific  written  consent  has  been  obtained,  in 
which  case  a copy  of  the  authorization  should  accompany  the 
manuscript.  Omit  illustrations  which  do  not  increase  understanding 
of  text.  Illustrations  must  be  limited  to  a reasonable  number  (four  il- 
lustrations should  be  adequate  fora  manuscript  of  4 to  5 typed  pages). 
The  following  information  should  be  typed  on  a label  and  affixed  to 
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ACKNOWLEDGMENTS  are  the  author's  prerogative;  however, 
acknowledgment  of  technicians  and  other  remunerated  personnel  for 
carrying  out  routine  operations,  or  of  resident  physicians  who  merely 
care  for  patients  as  part  of  their  hospital  duties  is  discouraged.  More 
acceptable  acknowledgments  include  those  of  intellectual  or  profes- 
sional participation. 

GALLEY  PROOFS  will  be  mailed  to  the  principal  author  for  correc- 
tions. Reprint  orders  forms  will  accompany  galley  proofs. 


NEW  MEMBERS 


Applications  for  membership  have  been  re- 
ceived from  the  following  physicians  by  the 
respective  parish  medical  societies  as  of  Jan- 
uary 13,  1988.  The  Louisiana  State  Medical 
Society  is  pleased  to  welcome; 

■ Calcasieu 

Dewey  D.  Archer  Jr,  MD 

2019  21st  St,  Lake  Charles  70601 

1983,  Tulane  University  School  of  Medidne 

psychiatry 

Jake  T.  Hollen,  MD 

North  Hwy  26,  Box  1027,  Jennings  70546 
1976,  University  of  Louisville  School  of 
Medicine 
internal  medicine 

Roger  M.  Williams,  MD 

2000  Oak  Park  Blvd,  Lake  Charles  70685 
1982,  LSU  School  of  Medicine,  Shreveport 
otolaryngology 

■ East  Baton  Rouge 

Randall  D.  Lea,  MD 

1759  Physicians  Park  Dr,  Baton  Rouge  70816 
1979>  LSU  School  of  Medicine,  New  Orleans 
orthopedics 

Jon  V.  Schellack,  MD 

5329  Didesse  Dr,  Baton  Rouge  70808 
1980,  LSU  School  of  Medidne,  New  Orleans 
vascular  surgery 

Mark  J.  Waggenspack,  MD 

1113  S Range  Ave,  Suite  B,  Denham  Springs 
70727 

1984,  LSU  School  of  Medicine,  New  Orleans 
pediatrics 

John  G.  Watts  111,  MD 

541  Shadows  Lane,  Suite  A,  Baton  Rouge 
70806 

1984,  Tulane  University  School  of  Medicine 
pediatrics 


■ Ouachita 

LaDonna  L.  Ford,  MD 

4801  S Grand,  Monroe  71201 
1984,  University  of  Arkansas  School  of 
Medicine 
internal  medicine 

Harvey  T,  Huddleston,  MD 

2601  River  Oaks  Dr,  Monroe  71201 
1962,  University  of  Mississippi  School  of 
Medidne 

obstetrics  & gynecology 

Alfred  D.  Tisdale,  MD 

1400  Auburn,  Monroe  71201 

1958,  Tulane  University  School  of  Medicine 

pathology 

■ Shreveport 

Charles  L.  Black,  MD 

2510  Bert  Koims  Loop,  Shreveport  71118 

1980,  LSU  School  of  Medidne,  Shreveport 
general  surgery 

David  A.  Cavanaugh,  MD 

940  Margaret  Place  #210,  Shreveport  71101 

1981,  LSU  School  of  Medidne,  Shreveport 
neurosurgery 

William  H.  Gallmaim  111,  MD 

PO  Box  44123,  Shreveport  71134 

1980,  Tulane  University  School  of  Medidne 

diagnostic  radiology 

Terry  W.  Kendrick,  MD 

909  OHve  St,  Shreveport  71104 

1984,  LSU  School  of  Medidne,  Shreveport 

pediatrics 


■ St.  Mary 

Rand  M.  Dooley,  MD 

608  First,  Morgan  City  70380 
1980,  Facultad  de  Medidna  de  la  Univer- 
sidad  de  Guadalajara,  Mexico 
obstetrics  & gynecology 

■ Tri-Parish 

Angela  J.  Gaskin,  MD 

402  E Green,  Tallulah  71282 

1982,  Meharry  Medical  College,  Nashville 

family  practice 

■ Vermilion 

Thomas  D.  Price,  MD 

710  North  Foote,  Kaplan  70548 

1978,  LSU  School  of  Medicine,  New  Orleans 

general  practice 

■ IntemI Resident  Members 

OUACHITA 

Jose  R.  Enriquez,  MD 

1701  McKeen  PI,  Apt  68,  Monroe  71201 
1975,  Faculty  of  Medidne  and  Surgery  Uni- 
versity of  Santo  Tomas,  Philipptnes 
family  practice 


JOURNAL  VOL  140  APRIL  3 


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ECG  OF  THE  MONTH 


I DON’T  REMEMBER  THE  NAME 

JORGE  I.  MARTINEZ-LOPEZ,  MD 


The  six  precordial  leads  shown  below  belong  to  a 64-year-old  man  and  were  recorded  shortly  after 
admission  to  the  hospital.  No  other  information  came  with  the  tracing. 


What  is  your  diagnosis?  Elucidation  is  on  page  7. 


JOURNAL  VOL  140  APRIL  5 


St  Stanislaiis 
helps  build  leaders. 


FOR  A FREE  BROCHURE  CALL  THE  DIRECTOR  OF  ADMISSI0NS-(601)  467-9057. 


“The  sense  of  moral  values  instilled  in  me  at 
St.  Stanislaus  has  been  the  cornerstone  of  my 

whole  adult  life” 


To  the  Brothers  of  the  Sacred  Heart,  every 
student  is  a potential  leader.  And  giving  him 
the  proper  example— spiritual,  intellectual 
and  moral  — is  our  mission  at  St.  Stanislaus. 


BOARDING  SCHOOL  GRADES  6-12 
SUMMER  CAMP  AGES  9-14 

304  South  Beach  Blvd.  Bay  St.  Louis,  MS  39520 


James  E.  Smith  graduated 
from  St.  Stanislaus  in  1945. 

He  went  on  to  serve  as  presi- 
dent of  T.  Smith  & Son,  Inc. 
of  New  Orleans  as  well  as  the  Dock  Board. 


^ W 


SAirJT  STTAIMISLALJS 


ECG  of  the  Month 

Case  presentation  is  on  page  5. 

DIAGNOSIS  — Ventricular  higeminy 

The  tracing  is  many  years  old,  but  it  was  pulled  from 
my  files  because  it  illustrates  important  points  worthy 
of  emphasis;  these  will  be  the  subject  of  the  discussion 
that  follows. 

DISCUSSION 

First  to  draw  the  attention  of  the  interpreter  when 
viewing  the  tracing  is  the  repetitive  pattern  of  cou- 
plets, consisting  of  two  QRS  complexes  of  different 
morphologies.  This  pattern  can  be  termed  ventricular 
bigeminy  and,  because  it  is  sustained,  ventricular  bi- 
geminal rhythm.  However,  bigeminy  is  not  an  ECG  di- 
agnosis; instead,  it  is  a descriptive  term  referring  to 
any  of  a number  of  disordered  cardiac  rhythms  char- 
acterized by  paired  impulses  separated  by  pauses. 
Bigeminal  rhythms  may  arise  from  ectopic  firing  or 
from  failure  of  impulse  formation  or  impulse  con- 
duction. Its  presence,  therefore,  should  evoke  a search 
for  its  many  causes  and  an  effort  to  define  its  precise 
mechanism.  Identification  of  the  mechanism  respon- 
sible for  bigeminal  rhythm  is  crucial  to  management: 
some  require  suppression,  some  require  artificial  car- 
diac pacing,  and  others  are  innocuous. 

Atrial  activity  is  depicted  by  the  presence  of  bi- 
phasic  (positive-negative)  sinus  P waves,  best  seen  in 
precordial  lead  VI.  The  P-P  interval  is  regular,  the 
sinus  rate  is  65  a minute,  and  the  P waves  march 
through  both  wide  QRS  complexes.  This  total  lack  of 
temporal  relationship  between  the  Ps  and  the  QRS 
complexes  is  referred  to  as  AV  dissociation.  But  this 
term,  as  is  the  case  with  bigeminy,  is  purely  descrip- 
tive and  requires  determination  of  its  cause  also. 

It  is  proper  now  to  analyze  further  the  QRS  com- 
plexes; this  will  be  done  by  using  precordial  lead  VI 
only.  Both  types  of  QRS  complexes  are  abnormal  in 
appearance  and  exceed  0.12  sec  in  duration,  but  it  has 
to  be  determined  whether  they  have  a supraventric- 
ular or  a ventricular  origin.  The  morphology  of  the 
QRS  complexes  in  VI  is  often  useful  in  making  this 
determination.  The  odd-numbered  QRS  complexes 
do  not  conform  to  the  classic  pattern  recorded  in  pure 
complete  right  bundle  branch  block;  instead,  they  have 


a monophasic  configuration  with  a notch  high  on  the 
upstroke  of  the  R wave  and  are  consistent  with  ectopic 
impulses  originating  in  the  left  ventricle.  By  contrast, 
the  even-numbered  QRS  complexes  in  lead  VI  do 
show  the  triphasic  pattern  typical  of  pure  CRBBB. 

This  finding  alone  is  a strong  indication  that  the  elec- 
trical impulses  responsible  for  the  even-numbered  QRS 
complexes  have  a supraventricular  origin  and  are  con- 
ducted downgrade  with  pure  CRBBB.  Thus,  the  first 
QRS  of  the  couplet  is  of  left  ventricular  origin  and  the 
second  of  supraventricular  origin. 

There  are  two  other  important  findings  in  lead 
VI.  One  is  that  a fixed  coupling  interval  exists  be- 
tween the  first  and  the  second  QRS  of  each  couplet. 

The  other  is  that  the  interval  between  the  second  QRS 
of  a couplet  and  the  first  QRS  of  the  next  couplet  is 
longer,  but  also  constant. 

The  interpreter  should  now  examine  lead  V4.  One 
should  detect  the  presence  of  small,  negatively-ori- 
ented spikes  that  recur  regularly  at  75  times  a minute. 
Closer  inspection  reveals  that  one  spike  occurs  im- 
mediately before  the  inscription  of  the  first  QRS  of 
the  couplet,  whereas  the  spike  that  follows  it  occurs 
on  the  upstroke  of  the  T wave  of  the  second  QRS  of 
the  couplet.  These  spikes  are  consistent  with  the  pres- 
ence of  an  artificial  cardiac  pacemaker;  the  sequences 
recorded  indicate  that  the  first  QRS  of  each  pair  is  a 
"paced  beat,"  whereas  the  second  is  not. 

Having  established  the  presence  of  an  artificial 
cardiac  pacemaker,  more  information  should  be  ex- 
tracted from  the  tracing:  the  location  of  the  pacing 
electrode(s),  whether  the  pacing  electrode  is  unipolar 
or  bipolar,  and  the  pacing  mode  of  the  pacemaker. 

The  first  QRS  of  each  pair  is  the  paced  QRS.  Because 
its  morphology  is  consistent  with  left  ventricular  ec- 
topy,  it  represents  left  ventricular  epicardial  pacing. 

The  small  amplitude  of  the  spikes  resulting  from  pace- 
maker firing  suggests  that  the  pacemaker  electrode  is 
either  bipolar  or  that  two  electrodes  are  present  in 
close  proximity  to  each  other  on  the  left  ventricular 
surface.  Finally,  because  the  pacemaker  fires  con- 
stantly and  does  not  sense  the  second  QRS  of  the 
couplet,  the  inescapable  conclusion  is  that  it  is  a fixed- 
rate  (VOO)  pacemaker. 

The  final  solution  to  this  tracing  can  now  be  sum- 
marized. First,  the  basic  cardiac  rhythm  is  sinus  at  65 
times  a minute.  Second,  AV  dissociation  is  present  ► 


JOURNAL  VOL  140  APRIL  7 


and  is  the  result  of  a functioning  artificial  cardiac  pace- 
maker. Third,  the  pacemaker  is  a fixed-rate  mode,  is 
stimulating  the  left  ventricular  epicardium  at  75  times 
a minute,  and  is  responsible  for  the  first  QRS  of  each 
couplet.  Finally,  the  second  QRS  of  each  couplet  rep- 
resents an  AV  junctional  premature  impulse  — very 
likely  the  result  of  reentry  — that  is  conducted  an- 
terograde with  CRBBB. 

Left  ventricular  stimulation  was  performed  many 
years  ago  by  inserting  the  pacing  electrode  directly 
into  the  ventricular  myocardium  using  open  chest 
surgery.  The  electrical  system  was  bipolar  and  con- 
sisted of  two  wires  inserted  in  close  proximity  to  each 
other.  The  ECGs  of  patients  in  whom  a left  ventricular 
epicardial  pacemaker  was  implanted  generally  show 
a RBBB  pattern  in  the  precordial  leads  and  right  axis 
deviation  in  the  frontal  leads.  Direct  left  ventricular 
stimulation  has  been  supplanted  by  pervenous  right 
ventricular  endocardial  stimulation. 

At  the  beginning  of  this  presentation,  I men- 
tioned that  this  was  an  old  tracing.  Upon  recognizing 


the  pacemaker  spikes,  the  reader  may  have  thought: 

'T  don't  remember  the  name  (of  the  pacemaker)  . . . 

but  the  pace  is  familiar."  ■ 

SELECTED  REFERENCES 

1.  Rubin  IL,  Arbeit  SR,  Gross  H:  The  electrocardiographic  recognition  of 
pacemaker  function  and  failiu-e.  Ann  Intern  Med  1969;71:603-615. 

2.  Castellanos  A Jr,  Ortiz  JM,  Fastis  N,  et  al:  The  electrocardiogram  in  pa- 
tients with  pacemakers.  Prog  Cardiovas  Dis  1970;12:190-209. 

3.  Castellanos  A,  Lemberg  L:  Pacemaker  arrhythmias  and  electrocardi- 
ographic recognition  of  pacemakers.  Circulation  1973;47:1382-1391. 

4.  Harthome  JW:  Indications  for  pacemaker  insertion:  Types  and  modes  of 
pacing.  Prog  Cardiovas  Dis  1981;23:393-400. 


Dr  Martinez-Lopez  is  a specialist  in  cardiovascular  diseases  affiliated 
with  the  Cardiology  Service,  Dept  of  Medicine  at  William  Beaumont 
Army  Medical  Center  in  El  Paso,  TX. 

The  opinions  and  assertions  contained  herein  are  the  private  views  of  the 
author  and  not  to  be  construed  as  official  or  as  reflecting  the  views  of 
the  Dept  of  the  Army  or  Dept  of  Defense. 


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8 JOURNAL  VOL  140  APRIL 


OTOLARYNGOLOGY/ 

HEAD  & NECK  SURGERY  REPORT 


IMMUNOTHERAPY  OF 
HEAD  AND  NECK  CANCER: 

AN  OVERVIEW 

ADRIAN  WILLIAMSON  III.  MD:  ROBERT  H.  MILLER.  MD 


Tumor  immunotherapy  has  become  a dynamic  area 
of  research  in  the  management  of  head  and  neck 
cancer.  With  rapid  developments  in  technology 
and  new  understanding  of  tumor  immunology,  the 
potential  for  immunological  intervention  in  cancer 
has  increased.  The  purpose  of  this  presentation  is 
to  provide  an  introduction  to  immunotherapy  of 
head  and  neck  cancer  with  a discussion  of  the 

various  modalities  used. 


Tumor  immunology  has  been  an  active  field  of  can- 
cer research  for  100  years.  The  field  of  tumor  im- 
munotherapy was  firmly  established  in  1943  by  Lud- 
wik  Gross  when  he  demonstrated  that  mice  of  a pure 
inbred  line  could  be  immunized  against  a tumor  that 
originated  in  the  same  line.^  Until  recently,  most  work 
in  immunotherapy  of  human  cancer  has  been  limited 
to  breast,  ovarian,  and  colon-rectal  cancer.  With  new 
understanding  of  tumor  immunology  and  improve- 
ments in  medical  technology,  the  field  has  grown  to 
include  all  aspects  of  oncology,  including  head  and 
neck  cancer. 

Immunotherapy  can  be  defined  as  ''the  admin- 
istration of  any  agent  or  treatment  which  stimulates, 
modifies,  or  restores  in  a specific  or  nonspecific  fash- 
ion host  immune  reactivity  and  results  in  the  regres- 
sion or  prophylaxis  of  tumors."^  Immunotherapy  can 
be  categorized  as  active  intervention,  adoptive  im- 
munotherapy, passive  immunotherapy,  or  immu- 
nodepletive  therapy  (Table). ^ 

Active  intervention  may  be  achieved  by  vacci- 
nation or  by  nonspecific  augmentation  of  the  immune 
system  with  an  immune  stimulant.  Although  there 
has  been  some  success  with  inducing  resistance  to  ► 


JOURNAL  VOL  140  APRIL  11 


IMMUNOTHERAPY 

Method 

Agents  Used 

Active  intervention 

specific  tumor  vaccine 
BCG 

C.  parvum 
levamisole 
thymic  hormones 
interferon 
interleukin  2 

Adoptive  immunotherapy 

leukocyte  clones 

Passive  immunotherapy 

monoclonal  antibodies 
antibody-toxin  conjugates 

Immunodepletive  therapy 

indomethacin 

cimetidine 

tumor  challenge  in  animals,  attempts  to  produce  use- 
ful vaccines  for  cancer  of  the  head  and  neck  have  been 
unsuccessful.^ 

Nonspecific  immune  system  stimulants  include 
bacillus  Calmette  Guerin  (BCG),  Corynebacterium  par- 
vum,  levamisole,  thymic  hormones,  and  lympho- 
kines.  BCG  is  employed  as  an  attenuated  strain  of  the 
bacillus.  It  has  been  shown  to  be  useful  in  animal 
models  with  a small  or  limited  tumor  burden,  and  it 
has  been  reported  to  prolong  survival  in  acute  mye- 
logenous leukemia.  However,  BCG  has  not  been  of 
significant  benefit  in  head  and  neck  cancer  therapy. 

Corynebacterium  parvum  contains  no  living  or- 
ganism and  is  made  from  phenol-killed  bacteria.  It 
has  been  shown  to  prolong  survival  in  breast  cancer 
and  small  cell  cancer  of  the  lung,  but  its  use  in  head 
and  neck  cancer  has  been  disappointing. 

Levamisole  is  an  anthelminthic  drug  that  appears 
to  enhance  the  immune  reactivity  in  organisms  whose 
immunity  is  impaired.  It  has  shown  limited  benefit 
in  patients  with  advanced  breast  and  lung  cancer  but 
it  does  not  appear  useful  in  head  and  neck  cancer. ^ 
Like  levamisole,  thymic  hormones  enhance  immunity 
only  when  the  immune  reactivity  is  impaired.  Thy- 
mosin a 1,  has  been  shown  to  enhance  in  vitro  pro- 
duction of  interleukin  2 (IL-2)  in  an  animal  model  but 
it  has  not  been  useful  in  clinical  trials. ^ 

Currently,  the  most  important  lymphokines  in 
immunotherapy  are  interferon  and  IL-2.  Interferon 
has  been  most  useful  in  the  treatment  of  laryngeal 
papilloma  where  up  to  85%  of  treated  patients  have 
shown  improvement  or  stabilization  of  their  disease.^ 


Recent  studies  of  IL-2  have  been  promising.  IL-2  has 
been  found  to  increase  cytolytic  T cell,  macrophage, 
and  natural  killer  cell  function  in  mice.  Head  and  neck 
cancer  patients  appear  to  be  deficient  in  T cells  that 
produce  IL-2.^ 

Adoptive  immunotherapy  is  the  transfer  of  tumor 
immunity  from  one  individual  to  another.  Most  work 
in  this  aspect  of  immunotherapy  is  directed  towards 
cloning  lymphocytes  from  a cancer  patient's  blood  or 
bone  marrow.  The  lymphocytes  could  be  stimulated 
to  develop  antitumor  properties  against  the  patient's 
tumor  and  then  reinjected  into  the  patient.  This  goal 
has  already  been  achieved  in  animal  models.^ 

Passive  immunotherapy  involves  administering 
antitumor  antibodies  to  patients  in  order  to  induce 
tumor  directed  cytotoxic  activity.  Most  work  in  this 
field  involves  the  use  of  monoclonal  antibodies.  These 
antibodies  are  produced  by  the  fusion  of  plasma  ceU 
tumors  with  normal  lymphocytes  that  have  been  stim- 
ulated against  a tumor  specific  antigen.  The  resulting 
tumor  specific  antibodies  can  be  used  in  several  ways. 
Monoclonal  antibodies  have  been  shown  to  enhance 
serologic  cytotoxic  factors  (such  as  complement) 
against  human  tumors.  Currently  there  is  much  in- 
terest in  attaching  cytotoxic  agents  to  the  antibody 
and  using  the  resulting  "magic  bullet"  to  cause  non- 
immunologic  killing  of  the  tumor  cells.  Finally,  mon- 
oclonal antibodies  are  being  used  in  diagnosis  of  poorly 
differentiated  head  and  neck  neoplasms  and  moni- 
toring tumor  recurrence.^ 

Immunodepletive  therapy  involves  reducing 
those  factors  that  are  immunosuppressive  or  inhibit 
expression  of  tumor  immunity.  These  factors  include 
prostaglandins,  blocking  antibodies,  and  suppressor 
cell  activity.  Prostaglandins  have  been  shown  to  cause 
suppression  of  NK  cell  activity,  decreased  cell  me- 
diated tumoricidal  function,  and  decreased  produc- 
tion of  lymphokines.  Up  to  60%  of  squamous  cell  head 
and  neck  cancer  patients  have  increased  levels  of  sup- 
pressor monocytes  that  produce  prostaglandin  £2-^ 
Some  trials  using  indomethacin  in  head  and  neck  can- 
cer patients  have  been  encouraging,  although  one 
study  using  an  animal  model  showed  increased  met- 
astatic disease  associated  with  indomethacin  ther- 
apy.^ 

An  increase  in  the  number  of  suppressor  T cells 
may  result  in  the  maintenance  of  certain  tumors.  It 
has  been  shown  that  suppressor  cell  activity  can  be 
blocked  with  cimetidine.  Some  trials  have  indicated 


12  JOURNAL  VOL  140  APRIL 


that  defects  in  cell  mediated  immunity  in  patients 
with  head  and  neck  cancer  can  be  reversed  with  ci- 
metidine  therapy.^ 

Other  factors  such  as  surgery,  conventional 
chemotherapy,  radiation  therapy,  blood  transfusions, 
and  poor  nutrition  can  result  in  decreased  immunity 
in  patients  with  head  and  neck  cancer.  All  of  these 
considerations  must  be  taken  into  account  when  eval- 
uating immunity  and  immunotherapy  in  head  and 
neck  cancer  patients.  ■ 

REFERENCES 

1.  Gross  L:  Intradermal  immunization  of  C3H  mice  against  a sarcoma  that 
originated  in  an  animal  of  the  same  line.  Cancer  Res  1943;3(5):326-333. 

I 2.  Suen  JY,  Myers  EN:  Cancer  of  the  Head  and  Neck.  New  York,  Churchill 
Livingstone,  1981. 

3.  Roitt  I,  Brostoff  J,  Male  D:  Immunology.  London,  Gower  Medical  Publish- 
ing Ltd,  1985. 

4.  Cummings  CW,  Krause  CJ:  Otolaryngology  — Head  and  Neck  Surgery.  St 
Louis,  CV  Mosby  Co,  1986,  Vol  1. 

5.  McQuarrie  DG:  Head  and  Neck  Cancer:  Clinical  Decisions  and  Management 
Principles.  Chicago,  Year  Book  Medical  Publishers  Inc,  1986. 

6.  Wolf  GT,  Schmaltz  S,  Hudson  J,  et  al:  Alterations  in  T-lymphocyte  sub- 
populations in  patients  with  head  and  neck  cancer.  Arch  Otolaryngol  Head 
Neck  Surg  1987;113(11):1200-1206. 

7.  Abemayor  E,  Kessler  DJ,  Ward  PH,  et  al:  Evaluation  of  poorly  differen- 
tiated head  and  neck  neoplasms.  Arch  Otolaryngol  Head  Neck  Surg 
1987;113(5):506-509. 


Dr.  Williamson  is  a resident  in  the  Dept  of  Otolaryngology-Head  & 
Neck  Surgery  at  Tulane  Medical  School  in  New  Orleans. 

Dr.  Miller  is  professor  and  chairman  of  the  Dept  of  Otolaryngology- 
Head  & Neck  Surgery  at  Tulane  Medical  School  in  New  Orleans. 

Reprints  will  not  be  available. 


I 


i 


1 


JOURNAL  VOL  140  APRIL  13 


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Jackie  Tucker,  LSMSA  President 


AUXILIARY  REPORT 


CONTINUITY  IS  THE  KEY 

SANCY  McCOOL;  JACKIE  TUCKER 


IMAGINE  A BUSINESS  that  Operated  on  the  principle 
that  each  fiscal  year  was  actually  a “new"  year,  and 
everything  had  to  be  evaluated  in  terms  of  starting  at 
the  very  begirming.  Not  only  is  it  hard  to  imagine 
someone  trying  to  have  a successful  operation  under 
such  circumstances,  but  it  is  equally  hard  to  imagine 
that  the  business  could  survive  for  very  long.  Just  as 
a house  grows  from  a foundation,  so  a business,  or 
an  organization,  grows  from  what  has  gone  before, 
coupled  with  fresh  and  innovative  ideas  derived  from 
the  new  leaders  each  year. 

We  like  to  feel  that  our  state  Auxiliary  has  buQt 
on  the  foundation  laid  and  labored  over  by  our  parish 
auxiliaries,  and  continues  to  grow  and  thrive  with 
input  from  our  national  leaders  and  state  officers.  Our 
leadership  seminars  both  within  Louisiana  and  at 
American  Medical  Association  (AMA)  Auxiliary  head- 
quarters in  Chicago  continue  to  inspire  and  encourage 
our  members  with  fresh  ideas.  Parish  auxiliary  visits 
by  our  Louisiana  State  Medical  Society  Auxiliary  pres- 
ident and  president-elect  each  year  give  members  a 
chance  to  talk  with  and  discuss  matters  of  importance, 
and  our  annual  state  meeting  gives  each  of  us  a chance 
to  evaluate  our  work  for  that  year,  and  make  plans 
to  improve  the  quality  of  the  functions  of  that  area  in 


the  year  to  come. 

Over  the  years,  service  needs  have  changed  for 
the  Auxiliary.  We  still  concentrate  heavily  on  health 
programs  and  projects  for  our  communities,  but  we 
now  also  stress  legislation,  aid  to  our  medical  schools 
through  AMA-Education  and  Research  Foundation, 
a support  system  for  our  members  and  their  physician 
spouses,  and  working  with  our  state  society  in  a team 
concept  of  care  and  involvement. 

With  the  demands  becoming  ever  greater  on  the 
medical  community,  it  is  imperative  that  we  keep  our 
organization  strong  and  viable.  Increased  member- 
ship to  fulfill  our  obligations  is  a "must,"  and  each 
physician  spouse  must  be  made  aware  of  the  necessity 
of  our  organized  efforts. 

The  foundation  is  strong,  the  leaders  are  dedi- 
cated, the  challenges  are  upon  us.  Now  it  is  up  to  all 
of  us,  as  individual  members,  to  make  the  dreams 
reality.  ■ 


Sancy  McCool  (wife  of  Dr  E.  Edward  McCool)  is  the  outgoing  president 
and  Jackie  Tucker  (wife  of  Dr  Robert  Tucker)  is  the  incoming  president 
of  Louisiana  State  Medical  Society  Auxiliary. 


JOURNAL  VOL  140  APRIL  15 


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Dale  Weaver 

2900  West  Fork  Drive,  Suite  200,  Baton  Rouge,  LA  70827,  (504)  291-1807 


June  20-23 

1st  International  Symposium  on  Orbital  Plastic  Siu^ery,  San 

Francisco.  Contact:  Plastic  Surgery  Educational  Foundation,  233 
N Michigan  Ave,  Suite  1900,  Chicago,  IL  60601;  (312)228-9900. 


July 


July  6-13 

Breast  Imaging  and  Ultrasound,  Alaska  88:  Cruise  the  In- 
land Passage.  Contact:  Medical  Seminars  International  Inc,  21915 
Roscoe  Blvd,  Suite  222,  Canoga  Park,  CA  91304;  (818)719-7380. 

July  14-16 

4th  Annual  Berkshire  Medical  Conference:  Advances  in  Car- 
diology, Hancock,  Massachusetts.  Contact:  Berkshire  AHEC, 
(413)447-2417. 

July  17-22 

Physicians  and  Their  Families:  Balancing  Commitments  to 
Family  and  Profession,  Estes  Park,  Colorado.  Contact:  Jayne 
Roberts,  Conference  Coordinator,  Division  of  Continuing  Educa- 
tion, The  Menninger  Clinic,  Box  829,  Topeka,  KS  66601-0829; 
(800)288-7377. 

July  19-23 

Louisiana  Academy  of  Family  Physicians  Annual  Scientific 
Assembly,  Sandestin  Beach  Hilton,  Destin,  Horida.  (Contact: 
LAPP,  4705  Iberville  St,  New  Orleans,  LA  70119. 

July  24-28 

34th  Annual  Southern  OB-GYN  Seminar,  Asheville,  North 
Carolina.  Contact:  Dr.  George  Schneider,  Ochsner  Clinic,  Dept 
of  OB-GYN,  1514  Jefferson  Hwy,  New  Orleans,  LA  70121; 
(504)838-4031. 

July  24-29 

8th  Aimual  Internal  Medicine  Review,  HQton  Resort,  South 
Padre  Island,  Texas.  Contact:  Scott  & White  Continuing  Medical 
Education  Office,  2401  South  31st  St,  Temple,  TX  76508; 
(817)774-2350. 

July  21  - August  2 
j Italy  and  the  Swiss  Alps,  Sponsored  by  INTRAV  and  the 
I Louisiana  State  Medical  Society.  Contact:  Anita  Bums,  LSMS, 

I 1700  Josephine  St,  New  Orleans,  LA  70113;  (504)561-1033, 

I (800)462-9508. 


August 


August  13-14 

Anesthesia  for  the  Cardiac  Patient  Having  Non-Cardiac 
Surgery,  San  Diego.  Contact:  American  Society  of  Anesthe- 
siologists, 515  Busse  Hwy,  Park  Ridge,  IL  60068. 

August  21-30 

INTRAV  Cruise  on  the  Queen  Elizabeth  2 and  London,  Con- 
tact: Anita  Bums,  Louisiana  State  Medical  Society,  1700  Josephine 
St,  New  Orleans,  LA  70113;  (504)561-1033,  (800)462-9508. 


September 


September  10-18 

4th  Annual  Fall  Ultrasound  Symposia,  London  and  Paris. 
Contact:  Annual  Fall  Ultrasound  Meeting,  Medical  Seminars  In- 
ternational Inc,  21915  Roscoe  Blvd,  Suite  222,  Canoga  Park,  CA 
91304;  (818)719-7380. 

September  14-19 

Cosmetic  Surgery  of  the  Face  and  Breast,  Monte  Carlo, 
Monaco.  Contact:  Francine  Leinhardt,  Conference  Coordinator, 
210  East  64th  St,  New  York,  NY  10021;  (212)838-9200  ext  2776. 

September  17-18 

Metropolitan  Regional  Refresher  Course,  Las  Vegas.  Con- 
tact: American  Society  of  Anesthesiologists,  515  Busse  Hwy,  Park 
Ridge,  IL  60068. 


October 


October  3-7 

6th  Annual  Comprehensive  Review  of  Vascular  Smgery, 

Santa  Monica,  C^ornia.  Contact:  UCLA  Extension,  PO  Box 
24901,  Los  Angeles,  CA  90024-0901;  (213)825-1901. 

October  8-12 

American  Society  of  Anesthesiologists  Annual  Meeting,  San 

Francisco.  Contact:  ASA,  515  Busse  Hwy,  Park  Ridge,  IL  60068. 


JOURNAL  VOL  140  APRIL  19 


IS  CANCER  SURVIVAL  POORER 
IN  LOUISIANA? 


VIVIEN  W.  CHEN,  PhD;  PELAYO  CORREA,  MD, 
JEAN  F.  CRAIG,  MS;  ELIZABETH  T.H.  FONTHAM,  DPH 


20  JOURNAL  VOL  140  APRIL 


Excess  cancer  mortality  for  selected  sites  has  been 
observed  in  Louisiana  since  the  early  30s.  At 
present  all  four  sex-race  groups  in  Louisiana 
experience  higher  mortality  rates  for  all  cancers 
combined  when  compared  to  the  national  averages. 
It  is  uncertain  whether  the  higher  death  rates 
result  from  higher  incidence  or  poorer  prognosis, 
or  a combination  of  both.  To  address  the  issue,  we 
examined  data  from  the  Louisiana  Tumor  Registry, 
Charity  Hospital  Tumor  Registry,  and  the 
Surveillance,  Epidemiology  and  End  Results 
program.  Three  measures  were  used  for 
comparison  between  the  state  and  national  data:  (1) 
incidence  and  mortality  rates,  (2)  incidence/ 
mortality  ratios,  and  (3)  relative  survival  rates. 
Poorer  survival  is  observed  for  New  Orleans  and  is 
more  evident  among  cancers  with  relatively  better 
prognosis.  Possible  reasons  for  this  unfavorable 
survival  include  socioeconomic  factors,  racial 
factors,  treatment  variation,  and  host  factors. 

Louisiana  has  been  singled  out  as  a community 
displaying  unusually  high  rates  of  cancer.  Since 
the  early  30s,  excess  mortality  rates  for  cancer  of  the 
oral  cavity  and  the  respiratory  system  have  been  ob- 
served. Between  1930  and  1932,  the  death  rate  for 
cancer  of  buccal  cavity  and  pharynx  in  Louisiana  white 
men  was  50%  higher  than  that  of  the  United  States 
(9.7  per  100,000  vs  6.3)  and  double  the  rate  (9.7  per 
100,000  vs  4.9)  for  the  southern  region  which  included 
the  states  of  Alabama,  Arkansas,  Florida,  Georgia, 
Kentucky,  Louisiana,  Mississippi,  North  Carolina, 
Oklahoma,  South  Carolina,  Tennessee  and  Virginia. 
Mortality  for  laryngeal  cancer  was  70%  higher  than 
the  national  rate  and  more  than  triple  the  rate  in  the 
south.  Lung  cancer,  a rare  cancer  then,  was  also  in 
excess  (4.0/100,000),  25%  higher  than  the  national  av- 
erage (3.2/100,000)  and  more  than  double  the  rate  for 
the  south  (1.7/100,000).!  . 

Death  rates  for  cancers  of  the  respiratory  tract, 
in  particular  lung  cancer,  have  risen  sharply  since 
1930,  both  in  Louisiana  and  nationwide  and,  since  the 
mid-50s,  have  become  the  leading  cause  of  cancer 
death  in  men.  The  lung  cancer  death  rate  in  Louisiana 
white  men  has  increased  tenfold  from  the  30s  (4.0/ 
100,000)  to  the  50s  (41.3/100,000)  and  doubled  from 
the  50s  to  70s  (80/100,000)  to  become  the  nation's  high- 
est lung  cancer  death  rate.  The  rate  of  increase  in  the 


United  States  was  similar  for  the  corresponding  pe- 
riods, from  3.2/100,000  to  29.6  to  64.0.^ 

Since  lung  cancer  became  the  leading  cause  of 
cancer  death  in  men  nationwide,  and  since  Louisiana 
showed  the  highest  lung  cancer  rate,  the  mortality 
rate  for  all  cancers  combined  in  Louisiana  white  males 
also  exceeded  the  national  rate  in  the  50s.  In  addition, 
cancer  mortality  of  all  sites  for  black  males  surpassed 
that  of  white  males  in  1964  to  become  the  highest 
among  the  four  sex-race  groups.  To  date,  mortality 
rates  for  all  cancers  combined  in  Louisiana  remain 
higher  than  the  national  averages  for  all  four  groups. 

Despite  the  consistent  observations  of  higher 
rates,  a question  remains  unanswered.  Are  the  ex- 
cessive cancer  death  rates  experienced  by  Louisiana 
residents  a result  of  a higher  risk  (ie,  higher  incidence 
rates),  a poorer  prognosis,  or  a combination  of  both? 
In  order  to  address  the  issue,  we  examine  data  from 
the  Louisiana  Tumor  Registry  (LTR),  the  Tumor  Reg- 
istry of  Charity  Hospital  at  New  Orleans,  the  End 
Results  Program  of  National  Cancer  Institute  (NCI), 
the  Surveillance,  Epidemiology  and  End  Results 
(SEER)  program  of  the  NCI  and  the  National  Center 
for  Health  Statistics.  Three  different  measures  are  used 
for  the  following  comparisons  between  national  and 
state  data:  (1)  incidence  and  mortality  rates,  (2)  inci- 
dence/mortality ratios,  and  (3)  relative  survival  rates. 

INCIDENCE  AND  MORTALITY  RATES 

Incidence  rates  are  the  best  estimates  of  cancer  risk 
in  a population.  The  LTR  has  been  collecting  inci- 
dence data  for  metropolitan  New  Orleans  (Jefferson, 
Orleans,  and  St  Bernard  parishes)  since  1974.  The 
registry  expanded  to  the  whole  southern  region  in 
1983,  to  the  northeast  region  in  1985,  and  to  the  Al- 
exandria and  Shreveport  areas  in  1987.  Since  it  takes 
several  years  to  accumulate  data  for  incidence  cal- 
culation, such  data  are  currently  available  for  the  New 
Orleans  area  only.  Therefore,  cancer  incidence  for  New 
Orleans  only  is  compared  to  the  national  averages, 
obtained  from  the  combined  experience  of  the  group 
of  population-based  registries  which  constitute  the 
SEER  program.  The  participants  include  five  entire 
states  and  five  metropolitan  areas:  Connecticut,  Iowa, 
New  Mexico,  Utah,  Hawaii,  Detroit,  Atlanta,  New 
Orleans,  Seattle-Puget  Sound  and  San  Francisco-Oak- 
land.^ 


JOURNAL  VOL  140  APRIL  21 


TABLE  1 

AVERAGE  ANNUAL  AGE-ADJUSTED  (US  1970  STANDARD)  INCIDENCE  AND  MORTALITY  RATE  PER  100,000  POPULATION 
AND  INCIDENCE/MORTALITY  RATIO  BY  PRIMARY  SITE,  RACE  AND  SEX  IN  NEW  ORLEANS  AND  ALL  SEER  AREAS 

(EXCLUDING  PUERTO  RICO),  1973-1977 

New  Orleans 

All  SEER  Areas 

Incidence 

Mortality 

I/M 

Incidence 

Mortality 

I/M 

All  sites 

WM 

412.4 

258.7 

1.59 

371.6 

209.5 

1.77 

WF 

270.8 

141.5 

1.91 

301.2 

136.9 

2.20 

BM 

480.8 

329.3 

1.46 

454.3 

292.1 

1.56 

BF 

282.3 

181.8 

1.55 

288.7 

160.6 

1.80 

Oral  Cavity 

WM 

22.3 

11.3 

1.97 

16.8 

5.8 

2.90 

& Pharynx 

WF 

6.6 

1.6 

4.13 

6.0 

2.0 

3.00 

BM 

26.8 

13.4 

2.00 

19.3 

9.0 

2.14 

BF 

8.2 

3.3 

2.48 

7.0 

2.5 

2.80 

Esophagus 

WM 

4.6 

5.8 

0.79 

4.8 

4.9 

1.00 

WF 

0.7 

1.0 

0.70 

1.6 

1.5 

1.07 

BM 

16.6 

12.4 

1.34 

16.9 

15.0 

1.13 

BF 

3.6 

2.7 

1.33 

4.5 

3.9 

1.15 

Stomach 

WM 

9.8 

6.9 

1.42 

12.7 

9.5 

1.34 

WF 

4.8 

4.5 

1.07 

5.6 

4.5 

1.24 

BM 

29.0 

21.4 

1.36 

22.4 

17.1 

1.31 

BF 

13.3 

10.9 

1.22 

9.9 

7.4 

1.34 

Colon 

WM 

37.1 

25.4 

1.46 

36.7 

21.3 

1.72 

WF 

27.3 

15.9 

1.72 

31.0 

16.9 

1.83 

BM 

31.5 

18.3 

1.72 

36.3 

20.9 

1.74 

BF 

30.9 

16.4 

1.88 

30.6 

17.4 

1.76 

Rectum 

WM 

20.4 

7.6 

2.68 

19.1 

5.7 

3.35 

WF 

9.6 

3.3 

2.91 

11.5 

3.3 

3.48 

BM 

17.0 

9.6 

1.77 

13.3 

6.3 

2.11 

BF 

9.3 

5.0 

1.86 

10.5 

3.6 

2.92 

Pancreas 

WM 

12.9 

11.7 

1.10 

11.9 

11.4 

1.04 

WF 

9.6 

8.5 

1.13 

7.7 

7.3 

1.05 

BM 

18.7 

14.4 

1.30 

17.5 

15.7 

1.11 

BF 

8.9 

7.8 

1.14 

11.9 

10.2 

1.17 

Larynx 

WM 

10.7 

3.6 

2.97 

8.3 

2.7 

3.07 

WF 

1.7 

0.4 

4.25 

1.3 

0.4 

3.25 

BM 

14.7 

3.3 

4.45 

12.1 

4.5 

2.69 

BF 

2.1 

0.5 

4.20 

1.9 

0.6 

3.17 

As  shown  in  Table  1,  New  Orleanians,  when 
compared  to  those  residing  in  the  SEER  areas,  display 
excessive  rates  for  certain  cancers  not  only  in  mortality 
but  also  in  incidence,  the  latter  indicating  a higher 
risk  of  acquiring  the  disease.  The  excessive  rates  in- 
clude; lung  cancer  for  all  four  sex-race  groups,  cancer 
of  the  oral  cavity  and  pharynx  for  all  except  white 
females,  cancer  of  all  sites  and  rectum  for  males  only, 
stomach  cancer  for  blacks  of  both  sexes,  and  cancers 
of  the  pancreas,  larynx,  bladder,  and  kidney  for  whites 
of  both  sexes.  Therefore,  the  observed  higher  mor- 
tality rates  are  at  least  in  part  the  result  of  a higher 
risk  of  acquiring  the  disease. 


Excessive  mortality  from  all  cancers  combined  is 
observed  for  white  females  in  New  Orleans  when 
compared  to  the  SEER  average  even  though  they  ex- 
perience a lower  incidence  rate.  Similarly,  lower  in- 
cidence contrasting  with  higher  mortality  is  observed 
for  breast  cancer  among  New  Orleans  women  (both 
black  and  white)  and  for  cancers  of  the  urinary  tract 
in  black  males.  These  findings  suggest  poorer  survival 
for  New  Orleans  patients  with  such  cancers. 

INCIDENCE/MORTALITY  RATIOS 

The  ratio  of  incidence  rate  to  mortality  rate  (I/M)  is  a 


22  JOURNAL  VOL  140  APRIL 


TABLE  1 (continued) 

New  Orleans 

All  SEER  Areas 

Incidence 

Mortality 

I/M 

Incidence 

Mortality 

I/M 

Lung 

WM 

107.6 

84.8 

1.27 

76.4 

62.5 

1.22 

WF 

27.4 

19.6 

1.40 

21.8 

16.2 

1.35 

BM 

129.6 

105.2 

1.23 

110.0 

92.6 

1.19 

BF 

27.5 

18.4 

1.49 

24.3 

17.6 

1.38 

Breast 

WF 

78.1 

28.7 

2.72 

85.6 

28.4 

3.01 

BF 

67.5 

30.3 

2.23 

72.0 

27.8 

2.59 

Cervix 

WF 

9.8 

2.9 

3.38 

10.9 

3.5 

3.11 

(invasive) 

BF 

24.4 

9.9 

2.46 

25.7 

10.5 

2.45 

Corpus 

WF 

12.5 

1.3 

9.62 

29.9 

1.9 

15.74 

BF 

13.3 

3.1 

4.29 

14.6 

3.1 

4.71 

Prostate 

WM 

55.7 

21.2 

2.63 

66.2 

22.0 

3.01 

BM 

100.8 

39.3 

2.56 

108.9 

41.1 

2.65 

Bladder 

WM 

32.9 

9.2 

3.58 

27.0 

7.7 

3.51 

WF 

8.6 

3.1 

2.77 

7.1 

2.2 

3.23 

BM 

11.8 

5.4 

2.19 

13.6 

5.3 

2.57 

BF 

5.1 

2.2 

2.32 

5.5 

3.4 

1.62 

Kidney 

WM 

10.9 

6.0 

1.82 

9.4 

4.4 

2.14 

WF 

4.8 

2.5 

1.92 

4.4 

2.0 

2.20 

BM 

7.5 

4.9 

1.53 

8.7 

4.2 

2.07 

BF 

3.2 

0.8 

4.00 

4.4 

1.8 

2.44 

Brain  & 

WM 

7.6 

5.1 

1.49 

6.7 

5.1 

1.31 

CNS 

WF 

4.6 

3.2 

1.44 

4.6 

3.3 

1.39 

BM 

4.3 

4.5 

0.96 

4.2 

3.4 

1.24 

BF 

3.7 

1.9 

1.95 

2.7 

1.9 

1.42 

Lymphoma 

WM 

14.2 

8.2 

1.73 

14.3 

7.7 

1.86 

WF 

10.4 

5.5 

1.89 

10.7 

5.2 

2.06 

BM 

8.4 

4.9 

1.71 

10.3 

5.6 

1.84 

BF 

5.1 

3.2 

1.59 

5.8 

3.2 

1.81 

Leukemia 

WM 

11.6 

9.9 

1.17 

13.0 

9.3 

1.40 

WF 

6.4 

5.2 

1.23 

7.7 

5.2 

1.48 

BM 

9.1 

8.9 

1.02 

11.1 

8.0 

1.39 

BF 

6.6 

7.0 

0.94 

6.8 

4.7 

1.45 

crude  measure  of  prognosis.  If  the  I/M  ratio  approx- 
imates one,  with  mortality  approaching  incidence,  it 
reflects  extremely  poor  prognosis.  On  the  other  hand, 
a high  I/M  ratio  indicates  good  prognosis. 

As  shown  in  Table  1,  I/M  ratios  for  many  cancer 
sites  are  lower  in  New  Orleans  than  in  the  SEER  areas. 
The  poorer  survival  is  more  evident  among  cancers 
which  in  general  have  good  prognosis  (ie,  cancer  of 
the  rectum,  female  breast,  uterine  corpus,  prostate, 
and  kidney).  For  cancers  with  very  poor  prognosis 
such  as  lung,  pancreas  and  stomach,  similar  ratios  are 


observed  between  New  Orleans  and  SEER  areas. 

In  addition,  lower  I/M  ratios  are  observed  among 
New  Orleans  blacks  when  compared  to  New  Orleans 
whites,  a phenomenon  which  is  consistent  with  the 
national  findings,  ie,  a poorer  survival  among  black 
cancer  patients.^' ^ 

Since  the  I/M  ratio  does  not  take  the  staging  of 
disease  into  account,  the  observed  poorer  survival  in 
New  Orleans  could  be  partially  explained  by  a larger 
proportion  of  patients  with  advanced  disease  at  the 
time  of  diagnosis. 


JOURNAL  VOL  140  APRIL  23 


BECAUSE 

ONIY 


ISAIWAYS 


REMEMBER  TO  WRITE  “DO  NOT  SUBSTITUTE.” 
IT  PROTECTS  YOUR  DECISION. 


Copyright  © 1987  by  Roche  Products  Inc.  All  rights  reserved. 


The  cut  out  "V"  design  is  a registered  trademark  of  Roche  Products  Inc. 


Charity  Hospital 

1 948- 1 984  National  Rates 

1950-1954*  1965-1969*  1977-1 981 1 


W 

B 

W 

B 

W 

B 

W 

8 

Esophagus 

2 

5 

8 

— 

5 

1 

22 

— 

Stomach 

39 

39 

42 

40 

40 

51 

75 

87 

Colon 

59 

60 

68 

54 

73 

65 

87 

85 

Rectum 

56 

51 

66 

40 

67 

55 

79 

69 

Pancreas 

5 

1 

1 

— 

5 

4 

— 

— 

Larynx 

67 

64 

68 

— 

79 

66 

— 

— 

Lung 

20 

15 

21 

23 

33 

21 

41 

36 

Breast 

71 

77 

83 

75 

85 

79 

96 

93 

Cervix 

74 

76 

75 

73 

78 

73 

84 

80 

Corpus 

77 

64 

84 

66 

86 

75 

92 

75 

Prostate 

50 

60 

60 

56 

70 

65 

85 

80 

Kidney 

54 

70 

57 

63 

68 

69 

— 

— 

Bladder 

60 

54 

67 

42 

72 

49 

87 

85 

Brain 

19 

24 

22 

27 

29 

31 

— 

— 

RELATIVE  SURVIVAL  RATE 

The  relative  survival  rate  is  generally  considered  the 
best  estimate  of  prognosis  for  cancer  patients.  It  is  the 
ratio  of  the  observed  survival  rate  to  the  expected 
survival  rate  for  persons  from  the  general  population 
who  are  similar  to  the  patient  group  with  respect  to 
age,  race,  sex  and  calendar  period  of  observation.  The 
relative  survival  rate  can  be  interpreted  as  an  estimate 
of  the  probability  of  escaping  causes  of  death  related 
to  the  diagnosed  cancer.  It  can  also  be  calculated  for 
specific  race,  sex,  and  stage  of  disease  at  diagnosis. 

In  order  to  compute  survival  rates,  active  follow- 
up of  each  patient  under  study  is  necessary.  Unfor- 
tunately, this  type  of  active  follow-up  is  extremely 
time-consuming  and  very  expensive,  and  is,  there- 
fore, usually  performed  in  hospital  settings  only.  The 
LTR  routinely  collects  only  passive  survival  infor- 
mation based  on  linking  mortality  computer  tapes  with 
the  master  incidence  file.  Charity  Hospital  at  New 
Orleans,  one  of  the  nation's  oldest  and  the  state's  first 
tumor  registry,  collects  active  follow-up  data.  It  began 


its  operation  in  1947  and  has  data  available  since  1948. 
Therefore,  it  is  selected  for  comparison  with  the  na- 
tional data. 

Table  2 presents  five-year  relative  survival  rates 
for  cancer  patients  in  Charity  Hospital  with  localized 
disease  only  and  compared  to  the  corresponding  na- 
tional figures.^  The  national  survival  rates  for  the  two 
earlier  periods,  1950-1954  and  1965-1969^  are  from  the 
previous  End  Results  Program  of  NCI  (which  has 
evolved  and  expanded  to  the  present  SEER  program) 
while  data  for  the  latest  period  come  from  SEER  reg- 
istries.^ Even  though  we  are  comparing  cancer  pa- 
tients with  the  same  stage  of  disease  (localized  dis- 
ease) and  by  race  (black  and  white  separately),  a poorer 
survival  is  observed  for  Charity  Hospital  patients  when 
compared  to  those  of  the  End  Results  Program  of  the 
NCI  and  the  SEER  program.  As  noted  previously,  the 
difference  is  more  marked  for  cancers  of  the  rectum, 
female  breast,  and  uterine  corpus. 

It  should  be  noted  that  the  survival  data  from 
Charity  Hospital  cover  a very  wide  range  of  time, 
during  which  major  breakthroughs  in  treatment  and  ► 

JOURNAL  VOL  140  APRIL  25 


improvement  in  survival  have  occurred.  However, 
due  to  the  lack  of  computer  support  at  the  Charity 
Hospital  Tumor  Registry  at  present,  comparisons  us- 
ing same  time-periods  are  not  possible.  Even  so,  when 
compared  to  the  national  rates  for  the  period  1950- 
1954,  survival  deficits  are  observed  for  Charity  white 
patients.  Since  Charity  patients  are  not  representative 
of  cancer  patients  in  Louisiana  at  large,  survival  data 
from  a more  comparable  private  hospital  was  ex- 
plored. Touro  Hospital  has  had  a tumor  registry  in 
operation  since  1958.  Unfortunately,  cases  diagnosed 
prior  to  1982  are  not  entered  in  a computer,  and  the 
available  data  consist  of  manually  computed  crude 
survival  rates  which  cannot  be  compared  with  the 
relative  survival  rates. 

DISCUSSION 

To  explore  the  reasons  for  the  poor  survival  in  Lou- 
isiana the  following  factors  should  be  taken  into  ac- 
count: 

1 . Socioeconomic  factors . 

Numerous  earlier  studies  have  suggested  socioeco- 
nomic factors  to  be  the  main  determinant  of  survival 
difference  among  cancer  patients.  "Low-income"  pa- 
tients do  not  do  as  well  as  the  "affluent"  private  pa- 
tients. Poorer  survival  rates  have  been  found  in  three 
studies  comparing:  low-income  with  high-income  pa- 
tients; non-private  or  indigent  hospital  patients  with 
private  patients;  and  public  hospital  patients  with  pri- 
vate hospital  patients. The  survival  deficit  remains 
even  after  adjusting  for  stage  of  the  disease,  treat- 
ment, and  quality  of  care.^^  The  data  shown  in  Table 
2 reflect  in  a major  way  socioeconomic  factors  because 
low  income  Charity  Hospital  patients  are  compared 
with  national  figures  in  which  higher  income  patients 
predominate. 

2.  Racial  factors. 

A black/white  survival  differential  in  cancer  patients 
has  been  observed  since  the  50s. The  large  survival 
disadvantage  for  black  patients  is  in  part  due  to  a 
higher  proportion  of  advanced  or  non-localized  dis- 
ease at  the  time  of  diagnosis,  confounded  further  by 
socioeconomic  factors.  Adjusting  for  age  and  stage  of 
disease  narrows  the  gap  of  overall  survival  rates  but 
falls  far  short  of  explaining  the  significant  black/white 
difference.®'  In  a 10-year  follow-up  study  on  breast 
cancer  patients  treated  at  M.D.  Anderson  Hospital, 


Westbrook  et  al  found  that  blacks  and  Chicanos  with 
"early"  diseases  had  a significantly  worse  survival 
rate  than  whites  with  the  same  stage  of  disease. 

3.  Treatment  variation. 

The  poorer  survival  among  public  hospital  patients  is 
generally  ascribed  to  lower  socioeconomic  status.  Since 
indigent  and  non-indigent  patients  are  usually  treated 
in  different  hospitals  and  by  different  medical  staffs, 
treatment  and  quality  of  care  variation  cannot  be  ex- 
cluded as  a prognostic  factor.  In  California  county 
hospitals,  attended  mostly  by  non-whites  and  lower 
socioeconomic  patients,  less  surgery  for  colon  cancer 
patients  was  performed  than  in  private  hospitals.^® 
Page  and  Kuntz^®  studied  the  survival  experience  of 
46,000  Veteran  Administration  (VA)  male  cancer  pa- 
tients and  found  no  significant  differences  between 
black  and  white  patients  except  for  bladder  cancer. 
They  suggested  that  their  findings,  which  differed 
from  those  in  other  studies,  were  due  to  the  fact  that 
all  veteran  patients  receive  the  same  treatment  with- 
out regard  to  socioeconomic  class  or  ability  to  pay. 
They  further  concluded  that,  when  treatment  and 
quality  of  care  were  the  same,  socioeconomic  factors 
and  race  do  not  generally  affect  survival  experience. 
However,  the  patient  population  seeking  care  at  VA 
hospitals  does  not  provide  the  same  contrast  existing 
between  private  and  Charity  Hospitals  clientele. 

4.  Host  factor. 

Host  differences  associated  with  poverty  have  been 
postulated  by  Berg  et  al  to  account  for  much  of  the 
observed  difference  in  survival  rates,  whether  it  is 
between  black  and  white,  indigent  and  non-indigent, 
or  public  and  private  patients. He  studied  the  rela- 
tionship between  economic  status  and  survival  for 
numerous  types  of  cancer  among  patients  of  the  Uni- 
versity of  Iowa  Hospital  and  found  a substantial  sur- 
vival difference  between  indigent  patients  and  clinic- 
pay  patients.  These  two  groups  of  teaching  patients, 
almost  all  of  them  white,  received  the  same  quality 
of  care,  but  the  clinic-pay  patients  were  of  higher 
economic  status.  Differences  in  age  at  diagnosis  and 
stage  of  disease  were  estimated  to  account  for  less 
than  half  of  the  survival  deficit  in  the  indigents;  the 
rest  of  the  deficit  was  associated  with  the  low  eco- 
nomic status. 

The  association  between  indigency  and  poor  sur- 
vival may  be  a reflection  of  host  vulnerability.  Poor 
general  health  may  influence  the  choice  of  treatment 


26  JOURNAL  VOL  140  APRIL 


which  can  in  turn  affect  survival.  Low  income  may 
also  result  in  poor  nutrition  and  poor  biological  im- 
munocompetence . 

All  of  the  aforementioned  factors  are  interrelated 
and  are  possible  reasons  for  the  apparent  poorer  sur- 
vival in  Louisiana.  Approximately  30%  of  the  popu- 
lation in  Louisiana  is  black  and  a larger  proportion  of 
our  residents  have  income  below  the  poverty  level: 
18.6%  vs  14.0%  nationally. In  the  Ten  State  Nu- 
trition Survey,  low  intake  of  vitamin  A was  found  in 
southern  parishes  where  cancer  rates  were  high  and 
serum  vitarnin  C was  deficient  in  15%  of  the  low- 
income  residents. Research  on  the  effect  of  nutrition 
on  cancer  incidence  and  survival  in  Louisiana  is  much 
needed. 

Since  1985,  we  have  been  conducting  a study  to 
investigate  the  black/white  prognosis  difference  in 
New  Orleans  patients  with  cancer  of  the  breast,  colon, 
uterine  corpus,  or  urinary  bladder.  The  study  is  con- 
ducted in  collaboration  with  the  NCI  and  researchers 
in  Atlanta  and  San  Francisco.  The  study  attempts  to 
explore  the  racial  differences  in  nutrition,  smoking 
and  alcohol  consumption,  social  support  from  family 
and  friends,  symptom  recognition,  delay  in  seeking 
care  and  entering  the  health  care  system,  financial 
resources,  and  compliance  with  treatment  as  weU  as 
morphologic  characteristics  of  the  primary  tumor. 

Preliminary  analyses  of  the  study  show  that  a 
smaller  proportion  of  black  patients  recognize  cancer- 
related  symptoms,  as  compared  to  the  whites.  They 
also  delay  longer  before  seeking  care  and,  when  they 
do,  it  is  more  often  for  reasons  other  than  tumor- 
related  symptoms.  Furthermore,  there  is  some  indi- 
cation of  nutritrional  deficiency  among  the  black  pa- 
tients. We  hope  that  upon  completion  of  the  study, 
we  will  have  a better  understanding  of  the  reasons 
for  survival  differential,  not  only  between  black  and 
white  patients,  but  between  Louisiana  and  other  areas 
in  the  nation. 

In  conclusion,  it  would  appear  that  in  Louisiana 
the  high  incidence  of  cancer  and  the  poorer  survival 
of  cancer  patients  is  mostly  related  to  factors  linked 
with  low  socioeconomic  status  and  the  existence  of  a 
large  indigent  population.  ■ 

ACKNOWLEDGMENT 

We  would  like  to  take  the  opportunity  to  thank  the 
following  24  hospitals,  their  adrrdnistrators  and  med- 


ical staff,  for  participating  in  this  BlackAVhite  Prog- 
nosis Study.  These  include  all  hospitals  treating  can- 
cer patients  in  greater  New  Orleans  except  one.  They 
are:  Chalmette  General  Hospital,  Charity  Hospital  at 
New  Orleans,  De  La  Ronde  Hospital,  Doctor's  Hos- 
pital, East  Jefferson  General  Hospital,  ELmwood  Med- 
ical Center  (formerly  Bonnabel  Hospital),  Flint-Good- 
ridge  Hospital  (1985  only).  Hotel  Dieu  Hospital, 
Humana  Woman's  Hospital,  Lakeside  Hospital,  Mea- 
dowcrest  Hospital,  Mercy  Hospital,  Montelepre  Me- 
morial Hospital,  New  Orleans  General  Hospital, 
Ochsner  Foundation  Hospital  and  Clinics,  Pendleton 
Memorial  Methodist  Hospital,  Jo  Ellen  Smith  Me- 
morial Hospital,  Southern  Baptist  Hospital,  St  Jude 
Hospital,  Touro  Infirmary,  Tulane  Medical  Center, 
United  Medical  Center,  Veteran  Administration  Hos- 
pital at  New  Orleans,  and  West  Jefferson  General 
Hospital.  In  addition,  we  are  grateful  for  the  partic- 
ipation of  private  radiation  centers  and  private  pa- 
thology laboratories.  We  also  would  Hke  to  extend 
our  appreciation  to  aU  clinicians,  especially  surgeons 
and  oncologists,  whose  cooperation  and  support  are 
essential  for  this  study.  Special  thanks  go  to  the  staff 
of  the  medical  records  department  and  pathology  de- 
partment of  each  hospital;  without  their  assistance, 
the  study  would  have  been  an  impossible  task  for  our 
research  team. 

This  work  was  supported  by  Grant  #N01-CP- 
43262  and  Contract  #N01-CN-45175. 


REFERENCES 

1.  Cover  M:  Cancer  Mortality  in  the  United  States,  III.  Geographic  Variation  in 
Recorded  Cancer  Mortality  for  Detailed  Sites,  for  an  Average  of  the  Years  1930- 
32,  Public  Health  Bulletin  No.  257.  US  Public  Health  Service,  1940. 

2.  Riggan  WB,  Van  Bruggen  J,  Mason  T,  et  al:  US  Cancer  Mortality  Rates 
and  Trends,  1950-79,  vol  1.  National  Cancer  Institute/Environmental  Pro- 
tection Agency,  1983. 

3.  Young  JL,  Percy  CL,  Asire  AJ:  Surveillance,  Epidemiology  and  End  Results: 
Incidence  and  Mortality  Data,  1973-77,  Dept  of  Health  and  Human  Services 
publication  No.  (NIH)  81-2330.  National  Cancer  Institute,  1981. 

4.  AxteU  LM,  Myers  MH:  Contrasts  in  survival  of  black  and  white  cancer 
patients,  1960-73.  JNCI  1978;60:1209-1215. 

5.  Sondik  E,  Yormg  JL,  Horm  JW,  et  al:  National  Cancer  Advisory  Board: 
Annual  Cancer  Statistics  Review.  Dept  of  Health  and  Hmnan  Services  1984. 

6.  Carter  RD,  Faddis  D,  Krementz  E,  et  al:  Charity  Hospital  Tumor  Registry, 
1948-84.  New  Orleans,  Charity  Hospital  of  Louisiana,  1986. 

7.  AxteU  LM,  Asire  AJ,  Myers  MH:  Cancer  Patient  Survival  Report  No.  5, 
Dept  of  Health,  Educational  Welfare  publication  No.  (NIH)  77-992, 1976. 

8.  Cancer  Registration  and  Survival  in  California.  Berkeley,  State  of  CaUfomia 
Dept  of  Public  Health,  California  Tumor  Registry;  1963. 

9.  Lipworth  L,  AbeUn  T,  CormeUy  RR:  Socioeconomic  factors  in  the  prog- 
nosis of  cancer  patients.  } Chronic  Dis  1970;23:105-115. 

10.  Lipworth  L,  Bennett  R,  Parker  P:  Prognosis  of  nonprivate  cancer  pa- 
tients. JNCI  1972;48:11-16. 


JOURNAL  VOL  140  APRIL  27 


11.  Berg  JW,  Ross  R,  Latourette  HB:  Economic  status  and  survival  of  cancer 
patients.  Cancer  1977;39A67-477 . 

12.  Myer  MH,  Hankey  BE:  Comparison  of  survival  for  black  and  white  pa- 
tients, in  Cancer  Patient  Survival  Experience.  Dept  of  Health  and  Human 
Services  PubUcation  No.  (NIH)  80-2148,  1980. 

13.  Myer  MH:  Survival  from  cancer  by  blacks  and  whites,  in  Cancer  Among 
Black  Populations,  Mettlin  C,  Murphy  GP  (eds).  New  York,  Alan  R Liss 
Inc  1981. 

14.  Westbrook  KC,  Brown  BW,  McBride  CM:  Breast  cancer:  A critical  review 
of  a patient  sample  with  a ten-year  follow-up.  South  Med  J 1975;68:543- 
548. 

15.  Krain  LS:  Racial  and  socioeconomic  factors  in  colon  cancer  mortality. 
Oncology  1972;26:335-344. 

16.  Page  WF,  Kuntz  AZ:  Racial  and  socioeconomic  factors  in  cancer  survival. 
Cancer  1980;45:1029-1040. 

17.  1980  Census  of  Population:  General  Social  and  Economic  Characteristics  — 
Louisiana,  PC80-1-C20.  US  Dept  of  Commerce,  Bureau  of  the  Census, 
1983. 

18.  Health  Status  of  Minorities  and  Low  Income  Groups.  Dept  of  Health  and 
Human  Resources  publication  No.  (HRSA)  HRS-P-DV  85-1.  Health  Re- 
sources and  Services  Administration,  1985. 

19.  Ten-state  nutrition  survey,  1968-70,  US  Dept  Health,  Education  and  Wel- 
fare 72-8129,  72-8130,  72-8131,  72-8132,  72-8133,  1972. 


Drs  Chen,  Correa,  and  Fontham  are  from  the  Dept  of  Pathology  at  LSU 
Medical  Center  in  New  Orleans.  Dr  Chen  is  also  affiliated  with  the 
Dept  of  Biostatistics  and  Epidemiology  at  Tulane  University  School  of 
Public  Health  and  Tropical  Medicine  in  New  Orleans. 

Ms  Craig  is  from  the  Louisiana  Tumor  Registry  in  the  Dept  of  Health 
and  Human  Resources  in  New  Orleans. 

Reprint  requests  should  be  sent  to  Vivien  W.  Chen,  PhD,  Dept  of 
Pathology,  LSU  Medical  Center,  1901  Perdido  St, 
New  Orleans,  LA  70112. 


28  JOURNAL  VOL  140  APRIL 


YOCON' 

YOHIMBINE  HCI 


Description;  Yohimbine  is  a 3a-15a-20B-17a-hydroxy  Yohimbine-16a-car- 
boxylic  acid  methyl  ester.  The  alkaloid  is  found  in  Rubaceae  and  related  trees. 
Also  in  Rauwolfia  Serpentina  (L)  Benth.  Yohimbine  is  an  indolalkylamine 
alkaloid  with  chemical  similarity  to  reserpine.  it  is  a crystalline  powder, 
odorless.  Each  compressed  tablet  contains  (1/12  gr.)  5.4  mg  of  Yohimbine 
Hydrochloride. 

Action:  Yohimbine  blocks  presynaptic  alpha-2  adrenergic  receptors.  Its 
action  on  peripheral  blood  vessels  resembles  that  of  reserpine,  though  it  is 
weaker  and  of  short  duration.  Yohimbine’s  peripheral  autonomic  nervous 
system  effect  is  to  increase  parasympathetic  (cholinergic)  and  decrease 
sympattietic  (adrenergic)  activity.  It  is  to  be  noted  that  in  male  sexual 
performance,  erection  is  linked  to  cholinergic  activity  and  to  alpha-2  ad- 
renergic blockade  which  may  theoretically  result  in  increased  penile  inflow, 
decreased  penile  outflow  or  both. 

Yohimbine  exerts  a stimulating  action  on  the  mood  and  may  increase 
anxiety.  Such  actions  have  not  been  adequately  studied  or  related  to  dosage 
although  they  appear  to  require  high  doses  of  the  drug . Yohimbine  has  a mild 
anti-diuretic  action,  probably  via  stimulation  of  hypothalmic  centers  and 
release  of  posterior  pituitary  hormone. 

Reportedly,  Yohimbine  exerts  no  significant  influence  on  cardiac  stimula- 
tion and  other  effects  mediated  by  B-adrenergic  receptors,  its  effect  on  blood 
pressure,  if  any,  would  be  to  lower  it;  however  no  adequate  studies  are  at  hand 
to  quantitate  this  effect  in  terms  of  Yohimbine  dosage, 
indications;  Yocon®  is  indicated  as  a sympathicolytic  and  mydriatric.  It  may 
have  activity  as  an  aphrodisiac. 

Contraindications:  Renal  diseases,  and  patient’s  sensitive  to  the  drug.  In 
view  of  the  limited  and  inadequate  information  at  hand,  no  precise  tabulation 
can  be  offered  of  additional  contraindications. 

Warning:  Generally,  this  drug  is  not  proposed  for  use  in  females  and  certainly 
must  not  be  used  during  pregnancy.  Neither  is  this  drug  proposed  for  use  in 
pediatric,  geriatric  or  cardio-renal  patients  with  gastric  or  duodenal  ulcer 
history.  Nor  should  it  be  used  in  conjunction  with  mood-modifying  drugs 
such  as  antidepressants,  or  in  psychiatric  patients  in  general. 

Adverse  Reactions:  Yohimbine  readily  penetrates  the  (CNS)  and  produces  a 
complex  pattern  of  responses  in  lower  doses  than  required  to  produce  periph- 
eral a-adrenergic  blockade.  These  include,  anti-diuresis,  a general  picture  of 
central  excitation  including  elevation  of  blood  pressure  and  heart  rate,  in- 
creased motor  activity,  irritability  and  tremor.  Sweating,  nausea  and  vomiting 
are  common  after  parenteral  administration  of  the  drug.T2  Also  dizziness, 
headache,  skin  flushing  reported  when  used  orally.T3 
Dosage  and  Administration:  Experimental  dosage  reported  in  treatment  of 
erectile  impotence.  ^ ^ 1 tablet  (5.4  mg)  3 times  a day,  to  adult  males  taken 
orally.  Occasional  side  effects  reported  with  this  dosage  are  nausea,  dizziness 
or  nervousness.  In  the  event  of  side  effects  dosage  to  be  reduced  to  Vi  tablet  3 
times  a day,  followed  by  gradual  increases  to  1 tablet  3 times  a day.  Reported 
therapy  not  more  than  10  weeks.3 
How  Supplied:  Oral  tablets  of  Yocon®  1/12  gr.  5.4  mg  in 


bottles  of  100’s  NDC  53159-001-01  and  1000’s  NDC 

53159-001-10. 

References; 

1.  A.  Morales  et  al..  New  England  Journal  of  Medi- 
cine; 1221 . November  12, 1981 . 

2.  Goodman,  Gilman  — The  Pharmacological  basis 
of  Therapeutics  6th  ed . , p . 1 76  - 1 88. 

McMillan  December  Rev.  1/85. 

3.  Weekly  Urological  Clinical  letter,  27:2,  July  4, 

1983. 

4.  A.  Morales  et  al. , The  Journal  of  Urology  128: 

45-47, 1982. 

Rev.  1/85 


AVAILABLE  EXCLUSIVELY  FROM 


PALISADES 

PHARMACEUTICALS,  INC. 

219  County  Road 
Tenafly,  New  Jersey  07670 

(201)  569-8502 
Outside  NJ  1-800-237-9083 


TOBACCO  AND  CANCER 


ELIZABETH  T.H.  FONTHAM,  DPH;  PELAYO  CORREA,  MD; 
VIVIEN  W.  CHEN,  PhD;  JEAN  F.  CRAIG,  MS; 

LINDA  W.  PICKLE,  PhD;  RONI  FALK,  MS 


Much  of  the  excess  cancer  risk  in  Louisiana  derives 
from  those  cancers  strongly  associated  with  tobacco 
use.  The  Cancer  Epidemiology  Research  Unit  of 
LSU  Medical  Center  Department  of  Pathology  has 
conducted  a series  of  studies  in  Louisiana  which 
examined  the  etiology  of  cancers  of  the  lung, 
stomach,  pancreas,  oral  cavity,  cervix,  and  bladder. 
Findings  indicate  that  approximately  90%  of  the 
lung  cancer  is  attributable  to  active  cigarette 
smoking.  Passive  smoke  exposure  was  found  to 
increase  risk  of  lung  cancer  one  and  one-half  to 
three-fold  among  non-smokers  married  to  smokers. 
Smoking  of  cigars  and  pipes  had  a more  consistent 
association  with  risk  of  stomach  cancer  than  did 
cigarette  smoking.  A significant  increasing  risk  of 
pancreatic  cancer  with  increasing  number  of 
cigarettes  smoked  was  seen.  Evidence  of  tobacco- 
induced  chromosome  damage  was  found  in 
epithelial  cells  from  the  oral  cavity,  urinary 
bladder,  and  uterine  cervix  consistent  with 
increased  risk  of  these  cancers  among  smokers. 


Any  consideration  of  chronic  disease  in  general, 
and  cancer  in  particular,  which  does  not  include 
the  role  of  tobacco  ignores  the  single  most  important 
causal  factor.  Recent  risk  estimates  indicate  that  to- 
bacco's contribution  to  all  cancer  deaths  is  approxi- 
mately 30%.^  The  only  other  factor  which  may  have 
an  impact  of  this  magnitude  on  cancer  causation  is 
diet.  Unlike  tobacco,  dietary  factors  may  exert  a pos- 
itive or  negative  effect  on  cancer  risk  and  will  be  dis- 
cussed separately  in  this  issue. 

What  are  the  tobacco-related  cancers  and  how  do 
Louisiana  rates  compare  with  the  rest  of  the  country? 
The  tobacco-related  cancers  are  listed  in  Table  1 with 
comparative  incidence  and  mortality  rates  for  the  race- 
sex  group  in  which  that  cancer  is  of  particular  im- 
portance. The  rates  for  each  cancer  for  all  sex-race 
groups  appear  in  the  preceding  article  {Is  cancer  sur- 
vival poorer  in  Louisiana?  by  Chen  et  al).  For  some  sites 
the  association  between  tobacco  use  and  cancer  is 
weU-documented  and  clearly  causal;  for  others,  the 
association  is  less  well  understood.  Almost  without 
exception,  Louisiana  tobacco-related  cancer  rates  are 
higher  than  the  rates  for  the  other  areas  of  the  United 
States.  The  most  striking  disparity  is  for  lung  cancer, 
which  alone  accounts  for  one-fourth  of  all  cancer 


JOURNAL  VOL  140  APRIL  29 


TABLE  1 

TOBACCO-RELATED  CANCERS;  MORTALITY  AND  INCIDENCE 


1970-1979  Average  Annual  Age 

1978-1981  Average  Annual  Age 

Adjusted  Mortality  Rates  Per  100,000 

Adjusted  Incidence  Rates  Per  100,000 

National 

Metropolitan 

Site 

Louisiana 

Average 

N.O. 

SEER* 

Lung  (WM) 

80.0 

64.0 

104.7 

81.0 

Larynx  (WM) 

2.9 

2.7 

12.9 

8.4 

Oral  Cavity  (WM) 

6.4 

5.2 

20.5 

16.8 

Esophagus  (BM) 

10.8 

12.3 

18.6 

t 

Bladder  (WM) 

6.9 

7.3 

28.6 

27.3 

Pancreas  (WM) 

12.9 

10.9 

12.5 

10.9 

Stomach  (BM) 

19.4 

16.2 

22.4 

21.3 

Cervix  (BF) 

11.6 

10.2 

20.0 

20.2 

* SEER:  Surveillance  Epidemiology  End  Results,  a continuing  project  of  the  National  Cancer  Institute  which  funds  population-based  tumor 
registries  at  various  sites  throughout  the  United  States, 
t Not  available 


deaths  in  this  country.  Incidence  and  mortality  rates 
in  Louisiana  are  25%  higher  than  in  other  areas  of  the 
country.  Lung  cancer  incidence  rates  in  New  Orleans 
for  black  males  are  the  highest  on  record  internation- 
ally: 107/100,000  per  year  (adjusted  to  the  "'world" 
population);  or  13.6  cumulative  rate  ages  0-74,  roughly 
indicating  that  approximately  13.6%  of  black  males  in 
New  Orleans  wUl  develop  lung  cancer. ^ 

Since  the  late  70s,  a number  of  epidemiologic 
studies  which  focused  on  the  etiology  of  these  cancers 
have  been  conducted  in  Louisiana.  The  main  findings 
of  these  studies  as  related  to  tobacco  will  be  briefly 
discussed. 

ACTIVE  SMOKING 

Lung  Cancer 

A survey  of  adult  males  in  south  and  north  Louisiana 
was  conducted  to  explore  lifestyle  and  environmental 
factors  which  might  explain  the  high  cancer  rates  in 
the  southern  part  of  the  state  compared  to  the  north- 
ern part.^  The  proportion  of  current  smokers  and  the 
level  of  non-filter  cigarette  use  were  both  higher  in 
south  Louisiana.  Smokers  in  the  southern  region  re- 
ported starting  at  an  earlier  age  than  their  northern 
counterparts.  In  addition,  a larger  proportion  of  whites 
living  in  the  south  reported  that  their  parents  had 

30  JOURNAL  VOL  140  APRIL 


smoked,  which  indicates  that  the  current  excess  of 
smokers  extends  back  at  least  one  generation.  These 
findings  suggested  that  at  least  one  factor  in  the  high 
lung  cancer  rates  seen  in  south  Louisiana  was  likely 
the  amount  and  manner  of  cigarette  smoking  in  that 
region. 

A case-control  study  of  lung  cancer  was  then  in- 
itiated in  a 26-parish  area  covering  south  Louisiana. 
Current  primary  lung  cancer  cases  were  identified 
from  hospital  admission  and  pathology  records  in 
hospitals.  All  the  major  hospitals  in  the  study  area 
participated  except  in  the  New  Orleans  metropolitan 
area  where,  by  design,  a sample  was  taken  of  the 
public  and  private  hospitals  accounting  for  approxi- 
mately half  the  lung  cancer  cases  in  the  city.  A control 
was  randomly  selected  from  patients  attending  the 
same  hospital  matched  by  race,  sex,  and  age  (within 
five  years).  Interviews  were  completed  for  1,253  cases 
and  1,274  controls,  representing  76%  and  85%  of  those 
eligible  respectively.  An  extensive  questionnaire  ob- 
tained information  concerning  tobacco  use,  diet,  oc- 
cupational, residential,  medical,  and  family  histories. 

As  noted  in  the  first  published  report  of  this  study, 
"in  terms  of  the  magnitude  of  risks  and  the  proportion 
of  the  population  exposed  to  the  risk  factors,  cigarette 
smoking  overshadows  all  other  factors."^  There  were 
few  cases  who  had  never  smoked:  97.7%  of  white 


TABLE  2 

ESTIMATED  RELATIVE  RISK  OF  LUNG  CANCER  ACCORDING  TO  HISTORY  OF  CIGARETTE  USE  BY  HISTOLOGIC  TYPE 

Number  of 
Cases 

All  Lung 
Cancers 

Squamous  and 
Small  Cell 
Carcinomas 

Adenocarcinomas 

Never  smoked 

51 

1.0 

1.0 

1.0 

Ever  smoked 

1201 

11.4 

28.3 

5.6 

Ex-smoker 

258 

6.5 

15.5 

3.7 

Current  smoker 

943 

14.2 

34.6 

6.7 

1 -20  cig/day 

371 

9.3 

23.2 

4.3 

21  -1-  cig/day 

514 

25.3 

54.8 

12.0 

male  lung  cancer  cases,  97.6%  of  black  males,  88%  of 
white  females,  and  94%  of  black  female  cases  had 
smoked.  Table  2 presents  the  risk  of  all  types  of  lung 
carcinoma  associated  with  cigarette  use  as  well  as  a 
separate  consideration  of  risk  by  histologic  type.  For 
heavy  current  smokers  in  Louisiana  the  risk  of  lung 
cancer  is  25  times  that  of  a non-smoker.  While  risk  of 
squamous  and  small  cell  carcinomas  (Kreyberg  I)  is 
clearly  the  most  striking,  a 12-fold  increased  risk  of 
adenocarcinoma  among  persons  smoking  more  than 
one  pack  a day  is  many  times  higher  than  any  other 
known  risk  factor  for  adenocarcinoma  of  the  lung. 

Estimates  of  relative  risk  of  lung  cancer  shown 
in  Table  3 indicate  increasing  risk  of  lung  cancer  for 
non-filter  only  versus  filter  only  relative  to  non-smok- 
ers. The  adverse  effects  of  depth  of  inhalation,  early 
initiation  of  cigarette  smoking,  and  failure  to  stop 
smoking  are  also  quantified.  While  other  risk  factors 
for  lung  cancer  have  been  delineated  by  this  study, 
estimates  of  attributable  risk  indicate  that  as  much  as 
90%  of  lung  cancer  in  this  region  is  attributable  to 
cigarette  smoking. 

Stomach  Cancer 

All  investigations  to  date  of  gastric  cancer  have  im- 
plicated diet  as  the  major  determinant  of  gastric  can- 
cer risk.  Smoking  has  been  examined  as  a risk  factor 
for  this  disease,  but  the  findings  have  been  equivocal. 
When  increased  risk  has  been  associated  with  smok- 
ing, no  dose  response  has  been  seen.^^  Because  of 
the  excessive  rates  of  stomach  cancer  among  south 
Louisiana  blacks,  a case-control  study  was  conducted 
concurrently  with  that  of  lung  cancer  utilizing  the 
same  study  design  and  interview.^  A total  of  391  cases 


TABLE  3 

ESTIMATED  RELATIVE  RISK  FOR  LUNG  CANCER  IN 
LOUISIANA  BY  SMOKING  CHARACTERISTICS 


Number  of  Adjusted* 

Cases  Relative  Risk 


Nonsmokers 

38 

1.0 

Filter 

51 

8.4 

Nonfilter 

395 

15.2 

Age  started 

<16 

604 

24.2 

16-20 

515 

17.4 

21  + 

167 

8.3 

Current  smoker 

1021 

12.6 

Quit 

3-5  years 

65 

7.7 

6-20 

154 

7.0 

20  + 

100 

3.9 

Inhalation 

None 

84 

4.6 

Mouth 

151 

6.3 

Chest 

1056 

11.3 

* Adjusted  for  sex  and  age 

Source:  Correa  P,  Pickle  L,  Fontham  E,  et  at;  The  causes  of 
lung  cancer  in  Louisiana,  in  Lung  Cancer:  Causes  and  Preven- 
tion, Mizeil  M,  Correa  P,  (eds).  Verlag  Chemie  International, 
Deerfield  Beach,  Fla  1984,  p 7^ 


and  matched  controls  were  included.  Table  4 presents 
estimates  of  relative  risk  of  stomach  cancer  associated 
with  tobacco  smoking.  Significantly  increased  risk  was 
associated  with  cigar  and  pipe  smoking  in  whites  and 
for  current  cigarette  smokers  among  blacks.  No  sig- 
nificant linear  trend  in  risk  was  found  for  number  of  ^ 

JOURNAL  VOL  140  APRIL  35 


TABLE  4 

ESTIMATED  RELATIVE  RISK  OF  STOMACH  CANCER 
ACCORDING  TO  TOBACCO  USE 


Adjusted  Relative 
Number  of  


Smoking  Status 

Cases 

Whites 

Blacks 

Non-smokers 

100 

1.0 

1.0 

Cigars  and/or 

28 

3.61t 

2.49 

pipe  only 

Cigarettes  only 

223 

1.28 

2.61 

Combined  types 

40 

0.95 

1.54 

of  smokers 

Ex-cigarette 

73 

1.04 

1.85 

smokers 

Current  cigarette 

190 

1.35 

2.66t 

smokers 


* Adjusted  for  age,  sex,  current  alcohol  consumption,  respond- 
ent status,  education  and  income 
Source;  Correa,  Fontham,  Pickle  et  al.  JNCI  75(4):645-654, 1985. 
t p < 0.05,  referent  non-smokers 


cigarettes  per  day,  pack-years  or  for  age  at  which 
smoking  began.  For  blacks  only,  an  increasing  risk 
was  found  with  increasing  duration  of  smoking.  A 
significant  inhalation  effect  was  found.  Deep  inhalers 
had  an  estimated  relative  risk  of  1.8  (p  < 0.05)  com- 
pared to  non-smokers  and  non-inhalers. 

The  failure  to  find  a dose-response  in  this  and 
other  studies  as  noted  suggests  that  the  association 
between  tobacco  use  and  stomach  cancer  is  not  a causal 
one.  It  is  possible  that  smoking  acts  as  an  irritant  and 
stimulator  of  acid  secretion,  facilitating  the  actions  of 
other  gastric  carcinogens. 

Pancreas  Cancer 

Results  of  the  case-control  study  of  pancreatic  carci- 
noma, the  third  cancer  site  in  the  three-pronged  in- 
vestigation of  excess  cancer  rates  in  Louisiana,  high- 
light cigarette  smoking  as  an  important  risk  factor  in 
southern  Louisiana.® 

A significantly  increasing  risk  with  increasing  cig- 
arette dose  was  seen  for  both  sexes  (Table  5).  No 
excess  risk  associated  with  the  limited  use  of  other 
tobacco  products  (cigars,  pipes,  snuff,  or  chewing  to- 
bacco) was  evident  in  this  study  population. 

36  JOURNAL  VOL  140  APRIL 


TABLE  5 

ESTIMATED  RELATIVE  RISK  OF  PANCREATIC  CANCER 
AMONG  CURRENT  SMOKERS  BY  SEX 


Cigarettes 
Per  Day 

Number  of 
cases 

Adjusted 
Relative  Risk* 

Males 

Females 

Never  smokers 

122 

1.0 

1.0 

1-15 

37 

1.31 

1.73 

16-25 

79 

2.02t 

1.82 

26  + 

59 

1.76t 

3.66t 

* Adjusted  for  age,  respondent  status,  income,  history  of  dia- 
betes mellitus,  coffee,  alcohol  and  fruit  consumption 
t p < 0.05,  referent  never  smokers 


Several  possible  mechanisms  of  pancreatic  car- 
cinogenesis by  cigarette  smoke  have  been  suggested: 
the  absorbed  carcinogens  may  reach  the  pancreas 
through  the  blood;  inactive  carcinogen  precursors  may 
be  activated  by  the  liver,  excreted  into  bile,  and  re- 
fluxed from  the  bile  duct  to  the  pancreatic  duct;  and 
finally,  smoking  may  elevate  blood  lipids,  which  in 
turn,  increase  the  risk  of  pancreatic  cancer.^ 

Cancers  of  the  Oral  Cavity,  Cervix,  and  Bladder 

Two  studies  conducted  at  Charity  Hospital  in  New 
Orleans  examined  the  tobacco-induced  cytogenetic 
damage  in  epithelial  cells  from  organs  which  have 
been  associated  with  increased  risk  of  cancer  in  smok- 
ers. 

Micronuclei  are  small  fragments  of  nuclear  ma- 
terial (DNA)  which  can  be  found  in  the  cytoplasm  of 
some  exfoliated  human  cells.  Formation  of  these  mi- 
cronuclei is  a marker  of  the  extent  of  recent  chro- 
mosome breakage,  when  the  cells  currently  being 
sloughed  were  dividing  in  the  basal  layer  of  epithe- 
lium. Micronuclei  in  exfoliated  human  cells  may  be 
used  as  an  in  vivo  marker  of  carcinogenic  exposure. 

The  first  study  included  486  patients,  each  of 
whom  submitted  a specimen  from  one  site  only  (buc- 
cal mucosa,  bronchus,  urinary  bladder,  or  uterine  cer- 
vix) and  answered  a brief  questionnaire  to  determine 
tobacco  and  alcohol  history  as  well  as  other  variables 
of  interest.  Significantly  elevated  proportions  of  mi- 
cronucleated  cells  were  found  for  smokers  compared 
to  non-smokers  in  each  of  these  tissues. 


TABLE  6 

FREQUENCY  OF  MICRONUCLEATED  CELLS  BY  SMOKING  STATUS  AND  SPECIMEN  TYPE 

Mean  % micronucleated  cells  (s.e.)* 

Urinary 

Uterine 

Buccal 

Bladder 

Cervix 

Mucosa 

Smokers 

0.46  (0.04) 

0.50  (0.03) 

0.47  (0.03) 

(n  = 99) 

Non-smokers 

0.08  (0.01) 

0.21  (0.02) 

0.08  (0.01) 

(n  = 101) 

p < 0.001 1 

p < 0.001 

p < 0.001 

* s.e.  = standard  error  of  the  mean 

t p values  from  standard  t-test,  smoker  vs.  non-smoker 

A follow-up  study  was  then  conducted  in  which 
exfoliated  cells  were  obtained  from  multiple  sites  in 
each  individual.  This  study  had  two  purposes:  (1)  to 
confirm  the  findings  of  the  pilot  study  of  an  increased 
proportion  of  micronuclei  among  cigarette  smokers 
compared  to  non-smokers  in  epithelial  cells  of  the  oral 
cavity,  bladder,  and  cervix,  while  controlling  for  other 
known  risk  factors  for  cancers  of  each  of  these  sites; 
(2)  to  examine  the  magnitude  of  cytogenetic  damage 
in  tissue  from  sites  which  have  direct  contact  with 
cigarette  smoke,  eg,  oral  cavity,  and  more  distant  sites 
which  do  not  have  direct  exposure,  such  as  the  blad- 
der and  the  cervix. 

The  data  presented  in  Table  6 demonstrate  to- 
bacco-induced chromosome  damage  in  buccal,  blad- 
der, and  cervical  tissues  consistent  with  increased  risk 
of  cancer  at  these  sites  among  smokers.  Within  the 
same  individual,  the  effect  was  of  similar  magnitude 
in  tissue  with  direct  contact  and  in  the  more  distant 
organs.  Even  after  controlling  for  cervical  cancer  risk 
factors  (age  at  first  intercourse,  number  of  sexual  part- 
ners, history  of  venereal  disease)  the  strong  tobacco 
effect  on  cervical  tissue  remained,  and  the  findings 
support  the  hypothesis  of  a causal  role  of  tobacco  in 
cervical  carcinogenesis. 

PASSIVE  SMOKING 

The  first  reports  suggesting  that  passive  or  involun- 
tary smoking  might  increase  risk  of  lung  cancer  in 
non-smokers  appeared  in  1981.^^'^^  The  first  report  of 
a significantly  increased  risk  of  lung  cancer  among 
non-smokers  married  to  a smoking  spouse  in  a US 
population  was  from  Louisiana. A two-fold  in- 


creased risk  was  found  for  non-smoking  men  and 
women  married  to  smokers.  The  estimated  relative 
risk  of  lung  cancer  Was  1.48  for  those  whose  spouse 
smoked  1-40  pack-years  and  3.1  for  those  whose 
spouse  smoked  more  than  40  pack-years  (p  < 0.05). 

Most  of  the  studies  of  passive  smoking  reported 
to  date  have  been  based  on  relatively  small  numbers 
of  cases.  For  example,  of  the  1,338  lung  cancer  pa- 
tients in  the  Louisiana  study,  only  30  (8  men  and  22 
women)  were  non-users  of  tobacco.  If  the  passive 
smoking  effect  is  specific  for  a particular  histologic 
type  as  has  been  suggested  by  recent  work,^^  then 
larger  sample  sizes  are  needed  to  estimate  risk.  It  is 
critical  to  include  only  lifetime  non-smokers  as  cases. 
Misclassification  of  only  a small  proportion  of  smok- 
ers as  non-smokers  could  elevate  the  estimate  of  rel- 
ative risk  to  the  levels  reported  because  active  smok- 
ers have  a risk  of  lung  cancer  many  times  greater  than 
true  non-smokers. 

In  order  to  study  passive  smoking  in  the  detail 
required  to  address  the  unanswered  questions,  a new 
study  was  initiated  in  January  1986,  centered  in  the 
Dept  of  Pathology  of  LSU  Medical  School.  In  collab- 
oration with  researchers  in  Atlanta,  Houston,  Los  An- 
geles, and  San  Francisco,  aU  newly  diagnosed  cases 
of  primary  lung  cancer  in  women  are  being  identified. 
The  combined  population  of  the  study  areas  is  ap- 
proximately 15  million  persons. 

The  earlier  Louisiana  lung  cancer  study  also  ex- 
amined the  association  of  parental  smoking  and  lung 
cancer  risk  in  their  adult  offspring  smokers. This 
study  did  not  demonstrate  an  association  between 
lung  cancer  risk  and  paternal  smoking.  There  was, 

JOURNAL  VOL  140  APRIL  37 


Physicians  Recognition  Award 


Eleven  physicians  from  the  state  of  Louisiana  were  awarded  the  Physicians  Recognition  Award  [PRA]  during 
January,  1 988.  This  award  is  presented  by  the  American  Medical  Association  to  physicians  who  have  voluntarily 
completed  150  hours  of  continuing  medical  education  during  a consecutive  three-year  time  period.  Of  these 
150  hours,  at  least  60  must  be  in  AMA/PRA  Category  1.  These  eleven  individuals  are  presented  below. 


Alexandria 

Alvin  Herbert  Honigman,  MD 


Baton  Rouge 

Tyrone  Thomas  Girod,  MD 


Lafayette 

Pamela  Susan  Darr,  MD 


New  Orleans 

Ana  Maria  Comaru-Schally,  MD* 
Michael  Patrick  Dolan,  MD 
Ronald  Lee  Nichols,  MD 
Chester  Bruno  Scrignar,  MD 
Kenneth  Lawrence  Veca,  MD 
Daniel  Keith  Winstead,  MD 

Shreveport 

Clarence  Elmo  Boyd,  MD 
Charles  C.  Schober,  MD 


* This  individual  is  not  a member  of  the  Louisiana  State  Medical  Society. 

The  criteria  for  PRA  are  planned  for  maximum  compatability  with  other  voluntary  or  required  CME  programs. 
Physicians  who  have  qualified  for  CME  programs  sponsored  by  the  following  medical  organizations  have  met 
the  requirements  for  the  AMA/PRA. 

American  Academy  of  Dermatology  (AAD) 

American  Academy  of  Family  Physicians  (AAFP) 

American  Association  of  Neurological  Surgeons/Congress  of  Neurological  Surgeons  (AANS/CNS) 
American  College  of  Obstetricians  & Gynecologists  (ACOG) 

American  College  of  Preventive  Medicine  (ACPM) 

American  Psychiatric  Association  (APA) 

American  Society  of  Clinical  Pathologists/College  of  American  Pathologists  (ASCP/CAP) 

American  Society  of  Colon  & Rectal  Surgeons  (ASCRS) 

American  Society  of  Plastic  & Reconstructive  Surgeons,  Inc.  (ASPRS) 

American  Urological  Association,  Inc.  (AUA) 

Arizona  Medical  Association,  Inc.  (ArMA) 

California  Medical  Association  (CMA) 

Medical  Society  of  the  District  of  Columbia  (MSDC) 

Medical  Society  of  New  jersey  (MSNj) 

Medical  Society  of  Virginia  (MSV) 

National  Medical  Association  (NMA) 

Pennsylvania  Medical  Society  (PMS) 

Physicians  who  have  qualified  within  the  last  3 years  for  the  certification  program  sponsored  by  CMA,  have 
met  the  requirements  of  AAD,  AAFP,  or  the  Continuing  Professional  Development  Program  (CPD)  of  ACOG 
may  receive  the  AMA/PRA  upon  request.  Physicians  who  qualify  for  the  ArMA/CME,  and  the  joint  ASCP/CAP 
Pathology  CME  Certificate  automatically  receive  the  PRA. 


38  JOURNAL  VOL  140  APRIL 


however,  approximately  a 40%  increased  risk  of  lung 
cancer  in  adult  offspring  smokers  associated  with  ma- 
ternal smoking;  and  this  association  persisted  after 
controlling  for  variables  indicative  of  active  smoking. 
These  findings  indicate  that  maternal  smoking  results 
in  a slight  increased  lung  cancer  risk  but  are  not  suf- 
ficient to  determine  whether  the  effect  is  a result  of 
enhanced  active  smoking  of  the  offspring  or  of  in- 
creased susceptibility  to  lung  cancer  induction  after 
the  challenge  of  active  smoking  in  later  life. 

Biologic  plausibility  of  a passive  smoke  effect  in 
lung  carcinogenesis  is  supported  by  laboratory  find- 
ings. Sidestream  smoke  (inhaled  by  nonsmokers) 
contains  much  higher  concentrations  of  toxic  and  car- 
cinogenic compounds  than  mainstream  smoke.  Ni- 
trosamines  (frequently  carcinogenic)  are  especially  ex- 
! cessive  in  sidestream  smoke. Nicotine  metabolites 
have  been  demonstrated  in  the  blood  and  urine  of 
adult  non-smokers  passively  exposed  to  cigarette 
smoke;  when  nitrosated,  they  are  carcinogenic.^^  In 
addition,  findings  from  a recently  completed  study  in 
New  Orleans  demonstrated  fetal  exposure  to  nicotine, 
cotinine  (the  major  metabolite  of  nicotine)  and  thio- 
cyanate, which  is  a good  indicator  of  nitrosation  po- 
tential. This  documentation  and  quantification  of  del- 
eterious components  of  tobacco  smoke  in  the  fetal 
environment  strengthens  the  already  weighty  argu- 
ment for  smoking  cessation  during  pregnancy. 

SMOKELESS  TOBACCO 

Use  of  chewing  tobacco  and  snuff  among  teenagers 
appears  to  be  increasing,  and  this  smokeless  tobacco 
is  a major  risk  factor  for  cancers  of  the  mouth  and 
throat.^®  These  cancers  usually  develop  at  the  site  di- 
rectly exposed  to  tobacco:  cigarette  smokers  develop 
more  throat  cancer  and  users  of  snuff  and  chewing 
tobacco  more  cancers  of  the  gum  and  buccal  mucosa. 
A 1986  Consensus  Development  Conference  spon- 
sored by  the  National  Institute  of  Health  estimates 
that  at  least  10  million  Americans  have  used  smoke- 
less tobacco  within  the  past  year,  including  three  mil- 
lion users  under  21  years  of  age.^®  The  need  to  address 
this  issue  is  apparent.  Mortality  rates  for  white  males 
throughout  the  state  currently  exceed  the  national 
average,  and  black  and  white  males  in  the  metropol- 
itan region  of  New  Orleans  have  the  highest  rates  in 
the  state.  Increased  use  of  this  type  of  tobacco  raises 
the  concern  of  increased  incidence  and  mortality 


from  oral  cancer  as  today's  youthful  users  reach 
adulthood.  ■ 

ACKNOWLEDGMENTS 

The  authors  wish  to  gratefully  acknowledge  the  par- 
ticipation of  the  following  institutions  in  one  or  more 
of  the  reported  studies:  Abbeville  General  Hospital, 
American  Legion  Hospital  — Crowley,  Baton  Rouge 
General  Hospital,  Charity  Hospital  of  New  Orleans, 
Doctor's  Memorial  Hospital,  East  Ascension  Parish 
Hospital,  Houma  Medical  and  Surgical  Clinic,  Iberia 
Parish  Hospital,  Intercommunity  Cancer  Center,  La- 
fayette General  Hospital,  Lake  Charles  Memorial 
Hospital,  Earl  K.  Long  Memorial  Hospital,  Huey  P. 
Long  Memorial  Hospital,  Louisiana  State  University 
Hospital,  Moosa  Memorial  Hospital,  Dr  Walter  O. 
Moss  Regional  Hospital,  Ochsner  Foundation  Hos- 
pital, Opelousas  General  Hospital,  Our  Lady  of  the 
Lake  Regional  Medical  Center,  Our  Lady  of  Lourdes 
Hospital,  Perkins  Radiation  Center,  Rapides  General 
Hospital,  St  Francis  Cabrini  Hospital,  St  Patrick  Hos- 
pital, Savoy  Memorial  Hospital  Foundation,  Schum- 
pert  Medical  Center,  Thibodaux  General  Hospital, 
Touro  Infirmary,  University  Medical  Center,  Veterans 
Administration  Hospital  — Alexandria,  Veterans 
Administration  Hospital  — New  Orleans,  Veterans 
Administration  Hospital  — Shreveport,  Ville  Platte 
General  Hospital,  West  Calcasieu-Cameron  Hospital. 

This  work  was  supported  by  contract  No.  NOl 
CP91023  of  the  National  Cancer  Institute  and  grants 
from  the  American  Cancer  Society,  the  Louisiana  State 
Board  of  Regents,  and  the  Louisiana  Cancer  and  Lung 
Trust  Fund  Board. 

REFERENCES 

1.  Doll  R,  Peto  R:  The  Causes  of  Cancer.  New  York,  Oxford  University  Press, 
1981,  p 1256. 

2.  Cancer  Incidence  in  Five  Continents,  vol  4.  Waterhouse  J,  Shanmugaratnam 
K,  Muir  C,  Powel  J,  (eds).  lARC  Sci  Pub  (42),  Lyon,  1982. 

3.  Correa  P,  Johnson  WD:  Cancer  and  lifestyle  in  Louisiana.  / La  State  Med 
Soc  1983;3:4-6. 

4.  Correa  P,  Pickle  LW,  Fontham  E,  et  al:  The  causes  of  lung  cancer  in 
Louisiana,  in  Lung  Cancer  Causes  and  Prevention.  Deerfield  Beach,  Fla, 
Verlag  Chemie  International,  1984,  pp  73-82. 

5.  Kahn  HA:  The  Dom  study  of  smoking  and  mortality  among  US  veterans: 
Report  of  8V2  years  of  observation.  Natl  Cancer  InstMonogr  1961;19:1-126. 

6.  Hirayama  T:  Epidemiology  of  stomach  cancer.  Jpn  J Cancer  Res  1971;11:3- 
19. 

7.  Correa  P,  Fontham  E,  Pickle  LW,  et  al:  Dietary  determinants  of  gastric 
cancer  in  south  Louisiana.  }NCI  1985;75:645-653. 

8.  Falk  R,  Pickle  LW,  Correa  P,  et  al:  Lifestyle  risk  factors  for  pancreatic 
cancer.  Am  } Epidemiol  1986;124:502. 

9.  Wynder  EL:  Ajn  epidemiological  evaluation  of  the  causes  of  cancer  of 
the  pancreas.  Cancer  Res  1975;35:2228. 


JOURNAL  VOL  140  APRIL  39 


specify  Adjunctive 


10.  Fontham  E,  Correa  P,  Rodriguez  E,  et  al:  Validation  of  smoking  history 
with  the  micronuclei  test,  in  Banbury  Report  23:  Mechanisms  in  Tobacco 
Carcinogenesis.  Cold  Spring  Harbor  Laboratory,  Cold  Spring  Harbor,  NY, 
1986,  pp  113-119. 

11.  Hirayama  T:  Nonsmoking  wives  of  heavy  smokers  have  a higher  risk  of 
lung  cancer:  A study  from  Japan.  Br  Med  } [Clin  Res]  1981;282:183-185. 

12.  Trichopolos  D,  Kalandidi  A,  Sparros  L,  et  al:  Lung  cancer  and  passive 
smoking.  Int  ] Cancer  1981;27:1-4. 

13.  Correa  P,  Pickle  LW,  Fontham  EH,  et  al:  Passive  smoking  and  lung 
cancer.  Lancet  1983;2:595-597. 

14.  Dalager  MA,  Pickle  LW,  Correa  P,  et  al:  Passive  smoking  and  lung  cancer 
among  non-tobacco  users.  Cancer  Res  1986;46:4808-4811. 

15.  Correa  P:  The  passive  smoking-cancer  controversy,  in  Banbury  Report  23: 
Mechanisms  in  Tobacco  Carcinogenesis.  Cold  Spring  Harbor  Laboratory, 
Cold  Spring  Harbor,  NY,  1986,  pp  343-360. 

16.  Weiss  ST,  Tager  IB,  Schenker  M,  et  al:  The  health  effects  of  involuntary 
smoking.  Am  Rev  Respir  Dis  1983;128:933-942. 

17.  Hoffman  D,  Hecht  SS:  Nicotine-derived  N-nitrosamines  and  tobacco- 
related  cancer:  Current  status  and  future  directions.  Cancer  Res  1985;45:935- 
944. 

18.  National  Institutes  of  Health  consensus  development  conference  state- 
ment: Health  implicahons  of  smokeless  tobacco  use.  CA  1986;36(5):310- 
316. 

19.  Smith  EM:  Epidemiology  of  oral  and  pharyngeal  cancers  in  the  US: 
Review  of  recent  Literature.  / Natl  Cancer  Inst  1979;63:1189-1198. 


Drs  Fontham,  Correa,  and  Chen  are  from  the  Dept  of  Pathology  at  LSU 

Medical  Center  in  New  Orleans. 

Ms  Craig  is  from  the  Louisiana  Tumor  Registry  in  the  Dept  of  Health 
and  Human  Resources  in  New  Orleans. 

Drs  Pickle  and  Falk  are  from  the  Environmental  Epidemiology  Branch 
of  the  National  Cancer  Institute,  in  Bethesda,  MD. 

Reprint  requests  should  be  sent  to  Elizabeth  Fontham,  MD, 
Dept  of  Pathology,  LSU  Medical  Center,  1901  Perdido  St, 

New  Orleans,  LA  70112. 


40  JOURNAL  VOL  140  APRIL 


(Hit) 




/TCP 


Each  capsule  contains  5 mg  chlordiazepoxide  HCl  and  2.5  mg 
clidinium  bromide 


Please  consult  complete  prescribing  information,  a summary  of  which 
follows: 


* 


Indications:  Based  on  a review  of  this  drug  by  the  National  Acad- 
emy of  Sciences— National  Research  Council  and/or  other  informa- 
tion, FDA  has  classified  the  indications  as  follows: 

“Possibly”  effeaive:  as  adjunctive  therapy  in  the  treatment  of  peptic 
ulcer  and  in  the  treatment  of  the  irritable  bowel  syndrome  (irntable 
colon,  spastic  colon,  mucous  colitis)  and  acute  enterocolitis. 

Final  classification  of  the  less-than-effective  indications  requires  fur- 
ther investigation. 


Contraindications:  Glaucoma;  prostatic  hypertrophy,  benim  bladder 
neck  obstruction;  hypersensitivity  to  chlordiazepoxide  HCl  and/or 
clidinium  Br. 

Warnings:  Caution  patients  about  possible  combined  effects  with  alco- 
hol and  other  CNS  depressants,  and  against  hazardous  occupations 
requiring  complete  mental  alertness  {e.g.,  operating  machinery,  driving). 
Physical  and  psychological  dependence  rarely  reported  on  recommended 
doses,  but  use  caution  in  administering  Librium®  (chlordiazepoxide  HCl/ 
Roche)  to  known  addiction-prone  individuals  or  those  who  might 
increase  dosage;  withdrawal  symptoms  (including  convulsions)  reported 
following  discontinuation  of  tne  drug. 

Usage  in  Pregnancy:  Use  of  minor  tranauilizers  during  first 
trimester  should  almost  always  be  avoided  because  of  uicreased 
risk  of  congenital  malformations  as  suggested  in  several  studies. 
Consider  possibility  of  premancy  when  instituting  therapy. 

Advise  patients  to  discuss  therapy  if  they  intend  to  or  do 
become  pregnant. 

As  with  all  anticholinergics,  inhibition  of  lactation  may  occur. 

Precautions:  In  elderly  and  debilitated,  limit  dosage  to  smallest  effective 
amount  to  preclude  ataxia,  oversedation,  confusion  (no  more  than 
2 capsules/aay  initially;  increase  gradually  as  needed  and  tolerated). 
Though  generally  not  recommended,  if  combination  therapy  with  other 
psychotropics  seems  indicated,  carefully  consider  pharmacology  of 
agents,  particularly  potentiating  drugs  such  as  MAO  inhibitors,  pheno- 
thiazines.  Observe  usual  precautions  in  presence  of  impaired  renal  or 
hepatic  funaion.  Paradoxical  reactions  reported  in  psychiatric  patients. 
Employ  usual  precautions  in  treating  anxiety  states  with  evidence  of 
impending  depression;  suicidal  tendencies  may  be  present  and  protective 
measures  necessary.  Variable  effects  on  blood  coagulation  reported  very 
rarely  in  patients  receiving  the  drug  and  oral  anticoagulants;  causal  rela- 
tionship not  established. 

Adverse  Reactions:  No  side  effects  or  manifestations  not  seen  with 
either  compound  alone  reported  with  Librax.  When  chlordiazepoxide  HCl 
is  used  alone,  drowsiness,  ataxia,  confusion  may  occur,  especially 
in  elderly  and  debilitated;  avoidable  in  most  cases  by  proper  dosage 
adjustment,  but  also  occasionally  observed  at  lower  dosage  ranges.  Syn- 
cope reported  in  a few  instances.  Also  encountered:  isolated  instances  of 
skin  eruptions,  edema,  minor  menstrual  irregularities,  nausea  and  con- 
stipation, extrapyramidal  symptoms,  increased  and  decreased  libido — 
all  infrequent,  generally  controlled  with  dosage  reduction;  changes  in 
EEG  patterns  may  appear  during  and  after  treatment;  blood  dyscrasias 
(including  agranulocytosis),  jaundice,  hepatic  dysfunction  reported 
occasionally  with  chlordiazepoxide  FICI,  making  periodic  blood  counts 
and  liver  function  tests  advisable  during  protracted  therapy.  Adverse 
effects  reported  with  Librax  typical  of  anticholinergic  agents,  i.e.,  dry- 
ness of  mouth,  blurring  of  vision,  urinary  hesitancy,  constipation.  Con- 
stipation has  occurred  most  often  when  Librax  therapy  is  combined 
with  other  spasmolytics  and/or  low  residue  diets. 


Roche  Products  Inc. 
Manati,  Puerto  Rico  00701 


PI.  0186 


DIET,  NUTRITION,  AND  CANCER 


PELAYO  CORREA,  MD;  ELIZABETH  FONTHAM,  DPH; 
VIVIEN  CHEN,  PhD;  JEAN  F.  CRAIG,  MS;  RONI  FALK,  MS; 

LINDA  W.  PICKLE,  PhD 


Results  of  three  case-control  studies  of  cancer  in 
Louisiana  are  presented,  addressing  dietary  and 
nutritional  factors  related  to  cancers  of  the 
stomach,  pancreas,  and  lung.  Smoked  and  cured 
meats  and  excessive  use  of  salt  were  found 
associated  with  an  increased  risk  of  gastric  cancer. 
Pork  products  were  associated  with  an  increased 
risk  of  pancreatic  cancer.  A common  finding  for 
cancers  of  the  stomach,  pancreas,  and  lung  is  that 
fresh  fruits  and  fresh  vegetables,  as  well  as 
vitamin  C and  beta-carotene,  appear  to  exert  a 

protective  effect. 


The  role  of  diet  and  nutrition  in  cancer  causation 
in  general  is  being  emphasized,  mostly  because  a 
wealth  of  recent  studies  have  uncovered  previously 
unsuspected  interrelationships,  summarized  in  a 
comprehensive  review  by  the  National  Academy  of 
Sciences.^ 

Louisiana  offers  a special  opportunity  to  study 
the  diet-cancer  relationship  because  of  the  unique  set- 
ting provided  by  the  different  racial  and  cultural  pop- 
ulation groups  (Cajuns,  Scotch-Irish,  blacks,  etc), 
which  have  preserved  their  own  dietary  patterns.  We 
have  recently  conducted  a series  of  epidemiologic 
studies  which  have  provided  information  of  interest 
in  this  area.  They  were  carried  out  thanks  to  the  ex- 
cellent collaboration  of  the  physicians  of  Louisiana 
who  allowed  us  to  interview  more  than  3,000  of  their 
patients  to  obtain  dietary  information.  The  authors 
consider  the  publication  of  the  results  a tribute  to  the 
Louisiana  physicians  who  have  made  this  research 
possible.  The  findings  are  here  summarized  and  dis- 
cussed in  the  light  of  cultural  idiosyncrasy  of  dietary 
habits  in  Louisiana. 


JOURNAL  VOL  140  APRIL  43 


LOUISIANA  POPULATION 

Both  cancer  and  diet  are  markedly  influenced  by  cul- 
ture, and  a few  words  about  the  Louisiana  population 
are  in  order.  Culturally,  there  is  more  than  one  Lou- 
isiana. Prominent  local  sociologists  who  have  studied 
the  subject  extensively  distinguish  coastal  Louisiana 
from  non-coastal  Louisiana.^  The  former  is  composed 
of  29  parishes  covering  42%  of  the  territory  and  67% 
of  the  population,  with  four  major  urban  centers,  and 
a younger  population  structure.  It  was  settled  mostly 
by  French-Canadians  (welcomed  by  the  then  Spanish 
government  of  the  state),  who  were  predominantly 
Catholic  and  not  too  committed  to  birth  control  prac- 
tices, and  who  became  "water-oriented"  for  food, 
livelihood  and  transportation.  This  contrasts  with  non- 
coastal Louisiana,  mostly  rural  and  Protestant,  more 
inclined  to  practice  birth  control,  settled  by  descen- 
dants of  Anglo-Saxon,  Scotch-Irish,  and  other  non- 
French  Europeans,  with  an  agricultural  structure  in- 
fluenced by  land  holding  patterns  prevalent  in  an- 
tebellum times.  Then  there  is  the  black  Louisiana  with 
its  own  cultural  characteristics  but  also  interacting  in 
different  ways  with  the  coastal  and  non-coastal  white 
populations,  and  in  both  cases  predominantly  occu- 
pying lower  socioeconomic  strata,  having  an  African- 
type  of  population  structure  with  a high  dependency 
index  (ratio  of  children  to  working  adults).^  The  high- 
est proportions  of  black  population  and  of  families 
below  poverty  level  are  concentrated  in  non-coastal 
Louisiana  and  especially  along  the  west  bank  of  the 
Mississippi  River. ^ 

DIET  IN  LOUISIANA 

Marked  differences  of  dietary  patterns  in  coastal  ver- 
sus non-coastal  whites  and  blacks  have  been  re- 
ported. The  eating  pattern  is  very  complex,  influ- 
enced in  each  subgroup  to  different  degrees  by 
accessibility,  family  needs,  and  social  prestige  of 
foods. ^ Typically,  north  Louisiana  whites  report  higher 
consumption  of  miscellaneous  vegetables,  potatoes, 
and  miscellaneous  fruits  when  compared  to  other 
groups.  South  Louisiana  whites  prefer  fish,  seafood, 
and  salads  more  than  other  groups.  Blacks  prefer  pork 
meats,  cornbread  and  rice.  The  diet  seems  more  var- 
ied in  the  north  than  in  the  south  in  both  races  but 
especially  in  whites.  Northern  whites  drink  tea  and 
citrus  fruits  while  southern  whites  prefer  beer.  Blacks 


prefer  soft  drinks.  Many  other  differences  have  been 
reported  by  the  scholarly  work  of  Steelman  which  was 
published  more  than  a decade  ago.^  No  recent  similar 
reports  are  known  to  the  authors  by  which  to  assess 
changes  that  may  have  taken  place  since  then  in  each 
of  the  four  sociocultural  groups.  But  the  data  of  Steel- 
man as  of  1974  provide  a rational  base  to  study  the 
influence  of  diet  on  cancer  in  these  subcultures.  This 
is  particularly  relevant  if  we  consider  that  cancer  rates 
at  the  present  time  are  influenced  by  exposures  ex- 
perienced years  before  because  of  the  prolonged  la- 
tency of  the  carcinogenesis  process.  We  published  in 
this  journal  the  results  of  a survey  of  adult  males  in 
north  and  south  Louisiana  (non-Cajuns  versus  Ca- 
juns) which  emphasizes  the  geographic  and  racial  dif- 
ferences in  diet,  including  alcohol  use.^ 

NUTRITION  IN  LOUISIANA 

Diet  provides  nutrients  and  non-nutrient  compo- 
nents, both  of  which  are  important  in  cancer  etiology. 
Several  national  nutritional  surveys  have  included 
Louisiana,  but  few  results  specific  for  Louisiana  sub- 
populations have  been  analyzed  and  published. 

Dietary  intakes  and  biochemical  indices  of  nutri- 
tional status  in  a sample  of  Louisiana  residents  were 
obtained  during  the  Ten-State  Nutrition  Survey,  1968- 
1970.^  Mean  intake  and  serum  levels  of  retinol  and 
beta-carotene  for  black  and  white  men  18  years  and 
older  were  calculated  for  19  parishes.  The  approxi- 
mate intake  in  the  northern  parishes  was  5,886  lU  of 
vitamin  A activity  while  the  corresponding  intake  for 
the  south  was  2,526  lU  — less  than  one  half.  Serum 
levels  of  vitamin  C were  deficient  and  low  in  15%  of 
low  income  and  9%  of  higher  income  Louisiana  res- 
idents. A strong  negative  correlation  between  serum 
levels  of  beta-carotene  and  vitamin  C and  lung  cancer 
mortality  rates  has  been  reported.^ 

The  Bogalusa  Heart  Study  is  an  epidemiologic 
investigation  of  the  early  natural  history  of  coronary 
artery  disease  and  hypertension  in  a biracial  pediatric 
population.®  As  part  of  this  study,  vitamin  intakes 
were  determined  in  10  and  13-year-old  children.  In 
four  sex-race  groups,  25%  to  50%  of  the  children  sur- 
veyed did  not  consume  the  recommended  daily  al- 
lowance (RDA)  of  vitamin  A,  thiamine,  and  ribo- 
flavin. Among  the  children  who  never  took 
supplemental  vitamins,  15%  to  36%  had  dietary  in- 
take of  vitamin  C less  than  one-third  of  the  RDA.  The 


44  JOURNAL  VOL  140  APRIL 


Whites 
Odds  Ratio 

Blacks 
Odds  Ratio 

Food  items 

Pork 

1.44 

1.35 

Rice 

1.34 

1.35 

Corn  bread 

1.32 

1.57 

Candy 

0.90 

2.12* 

Cake 

1.00 

1.56 

Coffee 

1.79 

0.90 

Salt 

1.17 

1.34 

Lettuce 

0.72 

0.52 

Tomato 

0.82 

0.56 

Banana 

0.73 

0.61 

Orange 

0.69 

0.89 

Fruit  juice 

0.74 

0.47 

Broccoli 

1.04 

0.50 

Food  groups 

Pork  products 

1.68* 

1.42 

Carbohydrates 

1.43 

0.76 

Sweets 

0.98 

1.88* 

Vegetables 

0.90 

0.70 

Fruits 

0.66 

0.65 

Vitamin  indexes 

Vitamin  C 

0.62* 

0.63 

Carotenoids 

0.68 

1.08 

Total  vitamin  A 

1.22 

0.85 

children  who  most  needed  an  ascorbic  acid  supple- 
ment were  the  least  likely  to  take  one.  These  findings 
for  children  and  adolescents  parallel  those  for  Loui- 
siana adults  in  the  sirrveys  noted  and  suggest  that 
the  problem  of  low  intake  of  key  micronutrients  is 
culturally  determined  at  an  early  age. 

STOMACH  CANCER 

Marked  changes  in  the  frequency  of  gastric  cancer 
have  been  observed  in  Louisiana.  Around  1950,  whites 
and  blacks  in  the  southern  portion  of  the  state  had 
rates  above  the  national  average.  The  excess  was  then 
shared  with  the  north  central  and  Rocky  Mountain 
states.^  A decade  later,  the  excess  in  south  Louisiana 
had  totally  disappeared  in  whites  but  persisted  in 
blacks.^®  There  is  scientific  consensus  in  assigning  diet 


as  the  overriding  cause  of  gastric  cancer,  which  should 
lead  to  the  conclusion  that  dietary  changes  have  oc- 
curred in  south  Louisiana  which  have  eliminated  the 
gastric  cancer  excess  in  whites  but  not  in  their  black 
counterparts  — an  interesting  subject  for  further  re- 
search. The  rates  are  also  declining  in  blacks,  but  since 
the  rates  in  south  Louisiana  blacks  are  stiU  higher  than 
those  of  other  blacks  in  the  country,  it  may  be  spec- 
ulated that  the  Cajun  influence  in  their  cooking  habits 
may  be  related  to  stomach  cancer. 

A case-control  study  was  conducted  recently  in 
which  391  patients  with  gastric  cancer  or  their  next- 
of-kin  were  interviewed  (126  white  males,  68  white 
females,  138  black  males  and  59  black  females).  A 
similar  number  of  controls  matched  by  sex,  age,  and 
race  were  also  interviewed.  The  study  covered  26  par- 
ishes in  south  Louisiana.  The  patients  were  diag- 
nosed, between  January  1979  and  March  1983,  as  hav- 
ing gastric  carcinoma.  A food  frequency  questionnaire 
including  59  items  was  administered,  emphasizing 
dietary  habits  prior  to  the  illness  under  study. 

A brief  summary  of  the  dietary  determinants  of 
risk  is  shown  in  Table  1 in  terms  of  odds  ratios  (OR), 
which  approximate  the  relative  risk  (RR)  associated 
with  each  factor,  given  a baseline  of  1.0  to  indicate 
lack  of  effect. 

In  addition  to  the  findings  shown,  consumption 
of  smoked  foods  (RR  1.70)  and  home  made  sausages 
or  home  cured  meats  (RR  2.32)  were  associated  with 
significant  increases  in  the  risk  of  stomach  cancer  in 
blacks. 

Alcohol  intake  was  also  associated  with  greater 
cancer  risk;  the  stomach  cancer  relative  risk  for  current 
drinkers  was  1.49  in  whites  and  1.66  in  blacks.  The 
consumption  of  fresh  fruits  and  vegetables  was  in- 
versely related  to  the  risk  in  whites  and  blacks  of 
south  Louisiana.  A dose-response  pattern  was  ob- 
served for  vitamin  C intake:  those  in  the  highest  quar- 
tile  of  consumption  had  a decreased  risk  (OR  0.33  in 
whites  and  0.50  in  blacks),  suggesting  a rather  strong 
protection  by  this  vitamin.  The  effect  of  carotenoids 
disappeared  when  vitamin  C was  controlled,  but  the 
effect  of  vitamin  C remained  after  controlling  for  other 
risk  factors,  including  carotenoid  intake. 

Salt  intake  is  a known  risk  factor  of  stomach  can- 
cer, and  excessive  salt  intake  appears  to  be  a char- 
acteristic of  south  Louisiana  diet.  Accurate  measures 
of  salt  intake  are  cumbersome  and  not  frequently  at- 
tempted. Houston  blacks  use  more  salt  than  whites,^^ 

JOURNAL  VOL  140  APRIL  45 


TABLE  2 

SIGNIFICANT*  DIETARY  DIFFERENCES  BETWEEN  BLACKS 
AND  WHITES  IN  SOUTH  LOUISIANA 

Consumption  higher  in  whites 

Consumption  higher 
in  biacks 

Shrimp 

Carrots 

Fish 

Oysters 

Eggplant 

Eggs 

Crabs 

Green  Beans 

Red  Beans 

Crawfish 

Corn 

White  beans 

Clams 

Lima  beans 

Rice 

Scallops 

Bananas 

Corn  Bread 

Milk 

Strawberries 

Spinach 

Cheese 

Other  fruits 

Sweet  potatoes 

Potatoes 

Canned  fruits 

Greens 

Pasta 

Preserves 

Okra 

Cereal 

Potato  chips 

Fruit  juice 

Bread 

Fritos 

Chicken 

Broccoli 

Popcorn 

Sausage 

Cabbage 

Cakes  and  pies 

Cold  cuts 

Lettuce 

Beef 

Organ  meats 

Squash 
Tomatoes 
Brussel  sprouts 

Ham 

Fresh  pork 

* p < .05  determined  by  Wilcoxon  rank  sum  test. 

and  excessive  salting  of  foods  by  blacks  is  a common 
observation  in  Louisiana  (again,  not  scientifically  doc- 
umented). In  our  study,  adding  salt  to  food  on  the 
table  was  associated  with  a risk  to  1.36  in  whites  and 
1.75  in  blacks.  Although  not  statistically  significant, 
these  observations  are  in  the  expected  direction,  as 
indicated  by  other  studies. 

The  pattern  emerging  from  this  study  suggests 
that  diet  is  the  main  determinant  of  gastric  cancer  risk 
in  south  Louisiana.  Food  items  associated  with  in- 
creased risk  include  some  that  are  very  popular  in  the 
region,  such  as  pork  meats,  smoked  meats,  home- 
cured  meats  and  sausage,  rice,  and  corn  bread.  Other 
popular  Louisiana  food  items,  such  as  crawfish,  oys- 
ters, shrimp,  and  crabs,  did  not  show  any  effect  on 
gastric  cancer  risk.  Items  associated  with  lower  risk 
consistently  fell  in  the  category  of  fresh  fruits  and 
fresh  vegetables. 

The  high  risk  of  gastric  cancer  in  south  Louisiana 
is  limited  to  blacks.  This  finding  led  to  a comparison 
of  the  dietary  patterns  of  blacks  and  whites.  The  com- 


parison was  achieved  by  pooling  the  data  for  controls 
in  three  large  case-control  studies  (lung,  pancreas, 
and  stomach)  that  had  been  conducted  simultane- 
ously in  south  Louisiana.  The  results,  summarized  in 
Table  2,  were  based  on  interviews  with  1,332  white 
and  686  black  residents  of  south  Louisiana.  Statisti- 
cally significant  black- white  differences  (p  < 0.05)  in 
the  frequency  distributions  of  consumption  are  pre- 
sented. The  comparisons  agree  with  our  findings  for 
the  relative  risks:  whites  (the  population  at  lower  risk) 
consume  more  vegetables,  salad  greens,  fresh  fruits 
and  dairy  products,  whereas  the  blacks  (the  popu- 
lation at  higher  risk),  consume  more  grains  and  starchy 
foods.  There  also  are  differences  in  the  sources  of 
animal  proteins  and  fat.  Blacks  have  a higher  con- 
sumption of  legumes  and  nitrite-preserved  meats,  such 
as  sausage  and  cold  cuts.  Possibly,  economic  reasons 
influence  these  food  patterns  inasmuch  as  the  foods 
preferred  by  whites  are  generally  more  expensive. 
This  possibility  is  consistent  with  the  well-known  in- 
verse correlation  between  economic  status  and  gastric 
cancer  risk  and  perhaps  with  the  time  trends  of  death 
rates  for  both  races  in  south  Louisiana. 

In  conclusion,  the  high  gastric  cancer  rates  in 
south  Louisiana,  especially  in  blacks,  may  be  linked 
to  the  effects  of  economy  and  traditional  dietary  pat- 
terns. Increased  risk  is  mostly  associated  with  smoked 
or  home-cured  meats,  alcohol,  and  probably  excessive 
salt  intake.  Lower  gastric  cancer  risk  is  primarily  as- 
sociated with  fresh  fruits  and  vegetables  with  their 
high  content  of  vitamin  C and  carotenoids.  A separate 
study  of  chronic  atrophic  gastritis  in  New  Orleans 
blacks  again  showed  a very  strong  inverse  association 
with  intake  of  vitamin  C and  fresh  fruits  and  vege- 
tables.^^ Chronic  atrophic  gastritis  is  considered  a pre- 
cursor of  gastric  carcinoma.  Changes  taking  place  in 
dietary  habits  are  likely  to  be  responsible  for  the  de- 
cline in  rates  observed  in  recent  decades.  The  above 
findings  may  offer  opportunities  to  accelerate  this  de- 
cline, especially  in  populations  at  highest  risk,  namely 
the  blacks  of  coastal  Louisiana. 

PANCREATIC  CANCER 

County-specific  cancer  maps  for  1950-1969  in  the 
United  States  showed  little  geographic  variation  ex- 
cept for  a cluster  of  parishes  with  high  rates  in  south- 
ern Louisiana,  particularly  among  white  males.^°  Of 
the  64  parishes  of  Louisiana,  25  had  death  rates  for 


46  JOURNAL  VOL  140  APRIL 


TABLE  3 

ADJUSTED  ODDS  RATIOS  FOR  PANCREATIC  CANCER 


Male  Female 

Servings/Month  Odds  Ratio  Odds  Ratio 


Breads  and  Cereals 
<32 
32-59 
60  + 

Beef 
<6 
6-15 
16  + 

Pork  Products 
<9 
9-30 
31  + 

Seafood 
<2 
2-7 
8 + 

Dairy 
<34 
34-67 
68  + 

Rice 
<4 
4-29 
30  + 

Fruits/Juices 
<25 
25-63 
64  + 

Vegetables 
<32 
32-73 
74  + 

Vitamin  Ct 
<2000 
2000-4455 
4456* 

Vitamin  A§ 

<18680 

18680-43577 

43578* 

Retinoi§ 

<11872 

11872-35631 

35632* 

Carotene§ 

<4436 

4436-9347 

9348* 


* p <0.05 

t Test  for  trend  p <0.05 

t Expressed  as  milligrams  per  month 

§ Expressed  as  the  number  of  retinoi  equivaients  per  month 


pancreatic  cancer  in  the  top  10%  of  all  US  counties 
for  white  males  and  10  had  rates  in  the  top  10%  for 
black  males.  More  recent  mortality  maps  for  the  70s 
showed  persistently  high  rates  in  south  Louisiana. 

Simultaneously  with  the  gastric  cancer  study  re- 
ferred to  above  and  utilizing  the  same  methodology, 
we  interviewed  363  cases  of  pancreatic  cancer  and 
compared  their  responses  to  those  of  1,234  subjects 
originally  identified  as  controls  for  the  pancreas, 
stomach,  and  lung  cancer  cases.  Details  of  the  study 
design  and  methodology  are  given  in  a separate  pub- 
lication.^^ 

Table  3 summarizes  the  findings  with  respect  to 
diet  and  nutrition,  presented  as  odds  ratios  adjusted 
for  age,  cigarette  smoking,  income,  residency,  history 
of  diabetes,  Cajun  ethnicity,  and  respondent  status 
to  avoid  confounding  by  these  factors. 

Elevated  risks  associated  with  frequent  con- 
sumption of  bread  and  cereal,  pork  products,  and  rice 
were  found.  Fruit  consumption  showed  a significant 
inverse  association.  The  risk  for  persons  reporting 
high  dietary  intake  of  vitamin  C was  38%  of  the  risk 
associated  with  low  intake  in  males  and  55%  in  fe- 
males. No  significant  effect  was  found  for  alcohol  or 
coffee  drinking. 

A study  of  food  interactions  revealed  an  inverse 
correlation  between  fruit  and  pork  intake.  High  fruit 
intake  diminished  the  risk  associated  with  pork  con- 
sumption while  low  fruit  and  juice  consumers  dis- 
played significantly  increased  risk  associated  with  pork 
intake.  Heavy  coffee  drinkers  were  very  low  con- 
sumers of  fruits,  and  an  elevated  risk  of  pancreatic 
cancer  among  heavy  coffee  drinkers  was  seen  only  in 
low  consumers  of  fruit.  This  may  be  considered  in 
evaluating  reports  of  elevated  risk  of  pancreatic  cancer 
in  heavy  coffee  drinkers  in  studies  in  which  the  con- 
sumption of  fruit  was  not  adequately  evaluated. 

The  influence  of  ethnicity  was  clear  for  some 
items.  Cajuns  tend  to  eat  fewer  fruits  and  more  rice 
than  non-Cajuns.  A strong  trend  of  increasing  risk 
for  pork  products  emerged  among  Cajuns  only.  The 
effect  of  vitamin  C was  stronger  among  Cajuns. 

Our  findings  concerning  the  antagonistic  effects 
of  pork  products  and  fruits  are  similar  for  stomach 
and  pancreatic  cancer.  This  suggests  similarities  in  the 
carcinogenesis  process  of  both  types  of  tumors.  We 
have  previously  suggested  intragastric  nitrosation,  and 
its  blockage  by  vitamin  C,  as  a possible  etiologic  model 
for  gastric  cancer. 


1.00 

1.00 

1.52* 

1.15 

1.26 

1.28 

1.00 

1.00 

1.19 

0.83 

1.08 

0.70 

1.00 

1.00 

1.39 

1.58 

1.72t 

1.26 

1.00 

1.00 

0.98 

1.22 

1.00 

1.87t 

1.00 

1.00 

1.55 

1.61 

2.18*t 

0.97 

1.00 

1.00 

0.94 

1.21 

1.46 

1.16 

1.00 

1.00 

0.62* 

0.58 

0.40*t 

0.46*t 

1.00 

1.00 

1.36 

1.09 

1.25 

1.33 

1.00 

1.00 

0.53* 

0.77 

0.38*t 

0.55t 

1.00 

1.00 

1.36 

1.09 

1.55 

1.13 

1.00 

1.00 

1.48 

0.94 

1.57t 

0.85 

1.00 

1.00 

0.99 

1.26 

0.82 

1.65 

JOURNAL  VOL  140  APRIL  47 


TABLE  4 


ADJUSTED  RELATIVE  RISK  OF  LUNG  CANCER  ASSOCIATED  WITH  ABOVE-MEDIAN 
CONSUMPTION  OF  SELECTED  FOOD  GROUPS 

All  Lung 

Squamous  & 

Cancers 

Small  Cell 

Adenocarcinoma 

Dairy  Products 

0.90 

0.90 

0.80 

Pork  products 

1.04 

1.04 

1.30 

Nitrite  meats 

1.03 

1.01 

1.12 

All  meats 

0.90 

0.98 

0.97 

Seafoods 

0.93 

0.86 

1.27 

Breads,  grains  & cereals 

1.04 

1.25 

0.70 

Vegetables 

0.79* 

0.79* 

0.70* 

Fruits 

0.77* 

0.73* 

1.00 

Fruits  & vegetables 

0.68* 

0.68* 

0.72* 

* p < .05 


LUNG  CANCER 

The  excess  of  lung  cancer  in  south  Louisiana  has  been 
amply  documented. The  monographs  of  the  Loui- 
siana Tumor  Registry  have  reported  on  incidence  and 
mortality  rates,  time  trends,  and  differences  by  age, 
sex,  and  geographic  location.^  It  has  been  estimated 
that  lung  cancer  accounts  for  85%  of  the  excess  of 
cancer  in  Louisiana  when  compared  to  the  United 
States. 

As  explained  above,  we  conducted  a case-control 
study  in  south  Louisiana  simultaneously  for  cancers 
of  the  lung,  stomach,  and  pancreas.  Interviews  with 
1,253  lung  cancer  patients  and  1,274  controls  yielded 
data  on  diet  and  nutrition  summarized  below.  Table 
4 shows  the  findings  for  selected  food  groups  by  his- 
tologic type,  adjusted  for  race,  sex,  age,  cigarette  use, 
family  income,  ethnic  group,  and  respondent  status 
in  order  to  avoid  confounding  of  the  results  by  these 
variables.  As  seen  in  the  table,  the  only  food  groups 
affecting  significantly  the  risk  of  lung  cancer  are  fruits 
and  vegetables,  which  are  associated  with  a lower 
risk.  Analysis  of  the  nutrient  content  of  food  revealed 
a significant  effect  of  vitamin  C and  carotene  for  squa- 
mous and  small  cell  carcinomas  but  not  for  adeno- 
carcinoma. Surprisingly,  lower  risk  associated  with 
retinol  intake  was  found  only  for  adenocarcinoma  and 
was  particularly  noteworthy  among  blacks. 

The  effects  of  carotene  and  vitamin  C are  found 
for  ex-smokers  and  current  light  smokers,  but  not  for 

48  JOURNAL  VOL  140  APRIL 


heavy  smokers  or  lifetime  non-smokers.  The  retinol 
effect  on  adenocarcinoma  was  most  pronounced  for 
current  heavy  smokers  but  its  significance  is  some- 
what compromised  by  the  fact  that  the  index  was 
heavily  dependent  on  the  intake  of  organ  meats,  and 
other  factors  associated  with  such  food  items  may  be 
confounding  the  retinol  effect  (unpublished  data). 

Vitamin  C intake  adjusted  for  carotene  intake  re- 
mains a risk-reducing  factor,  but  carotene  adjusted 
for  vitamin  C consumption  loses  its  protective  effect. 
The  same  results  were  observed  for  gastric  cancer.  It, 
therefore,  seems  that  vitamin  C may  be  the  most 
prominent  nutritional  factor  in  the  Louisiana  popu- 
lation (unpublished  data). 

CONCLUSIONS 

1.  Historical  facts  have  resulted  in  the  presence  of 
distinct  ethnic  and  geographical  dietary  patterns 
in  Louisiana. 

2.  These  dietary  patterns  may  have  an  influence  in 
the  peculiar  cancer  profile  of  Louisiana,  especially 
as  it  relates  to  high  rates  of  respiratory  and  diges- 
tive tract  neoplasms. 

3.  Dietary  items  associated  with  high  cancer  risk  in 
south  Louisiana  are  pork  meats,  smoked  and  home- 
cured  meats,  rice  and  corn  bread.  Excessive  salt 
intake  is  suspected  as  a factor  in  the  high  gastric 
cancer  rates  in  blacks. 

4.  Perhaps  the  most  interesting  and  potentially  im- 


portant  finding  is  that  the  Louisiana  diet  may  be 
less  than  optimal  in  its  supply  of  substances  that 
may  protect  against  cancer  development.  The  most 
prominent  nutrient  in  this  regard  is  vitairiin  C, 
which  may  be  of  special  importance  to  Louisiana's 
population.  Scurvy  is  not  a frequent  disease  in 
Louisiana,  which  illustrates  the  point  that  the  rec- 
ommended daily  allowance  (supposedly  sufficient 
to  prevent  scurvy)  is  not  the  best  measure  of  the 
adequacy  of  a nutrient  in  the  community.  Sub- 
optimal  carotene  intake  may  also  be  a prominent 
factor  related  to  the  high  cancer  rates  of  Louisiana. 

■ 

ACKNOWLEDGMENTS 

This  work  was  supported  by  contract  No.  NOl 

CP91023  and  Grant  No.  28842  of  the  Etiology  Branch 

National  Cancer  Institute. 

REFERENCES 

1.  Diet,  nutrition,  and  cancer.  National  Research  Council.  National  Academy 
Press,  1982. 

2.  Paterson  KW,  Lindsey  JL,  Bertrand  AL:  The  Human  Dimension  of  Coastal 
Zone  Development,  bulletin  No.  679.  Baton  Rouge,  La,  Louisiana  State 
University  Center  for  Agricultural  Sciences  and  Rural  Development,  1974. 

3.  Cancer  in  Louisiana,  vol  1 (1983),  2 (1985)  and  3 (1986).  New  Orleans,  La, 
Louisiana  Tumor  Registry,  Dept  of  Health  and  Hmnan  Resources,  Di- 
vision of  Administration  and  Louisiana  State  University  Graphic  Serv- 
ices. 

4.  Steelman  VP:  The  Cultural  Context  of  Food:  A Study  of  Food  Habits  and  Their 
Social  Significance  in  Selected  Areas  of  Louisiana,  bulletin  No.  679.  Baton 
Rouge,  La,  Louisiana  State  University  Center  for  Agricultural  Sciences 
and  Rmal  Development,  1974. 

5.  Correa  P,  Johnson  WD:  Cancer  and  lifestyle  in  Louisiana.  J La  State  Med 
Soc  1983;3:4-6. 

6.  Ten-state  Nutritive  Survey  1968-1970,  72-8129,  72-8130,  72-8131,  72-8132, 
72-8133.  US  Dept  of  Health,  Education  and  Welfare,  1972. 

7.  Lopez  A,  Yates  B,  Johnson  WD,  et  al:  The  role  of  vitamin  A and  ascorbic 
add  in  relation  to  respirator}'  system  cancers.  Abstracted,  Am  J Clin  Nutr 
1979;32:954. 

8.  Farris  RP,  Cresanta  JL,  Webber  LS,  et  al:  Dietary  studies  of  children  from 
a biradal  population:  Intake  of  vitamins  in  1(1-  and  13-year-olds.  J Am 
Coll  Nutr  1985;4:539-552. 

9.  Haerrszel  W:  Variation  in  inddence  and  mortality  from  stomach  cancer 
with  particular  reference  to  the  Uruted  States.  JNCI  1958,21:213-262. 

10.  Mason  TJ,  McKay  FW,  Hoover  R,  et  al:  Atlas  of  Cancer  Mortality  for  U.S. 
Counties:  1950-1969.  Washington,  DC,  Government  Printing  Office,  1975. 

11.  Kerr  GR,  Amante  P,  Decker  M,  et  al:  Ethnic  patterns  of  salt  purchase  in 
Houston,  Texas.  Am  J Epidemiol  1982;115:906-916. 

12.  Correa  P,  Fontham  E,  Williams  PL,  et  al:  Dietary  determinants  of  gastric 
cancer  in  south  Louisiana.  JNCI  1985;75:645-654. 

13.  Fontham  E,  Zavala  D,  Correa  P,  et  al:  Diet  and  chronic  atrophic  gastritis: 
A case-control  study.  JNCI  1986;76(4):621-627. 

14.  Falk  R,  William  PL,  Fontham  E,  et  al:  Lifestyle  factors  for  pancreatic 
cancer  in  Louisiana.  Am  J Epidemiol,  to  be  published. 


Drs  Correa,  Fontham,  and  Chen  are  from  the  Dept  of  Pathology  at  LSU 

Medical  Center  in  New  Orleans. 


Dr  Craig  is  from  the  Jjouisiana  Tumor  Registry  in  the  Dept  of  Health 
and  Human  Resources  in  New  Orleans. 

Drs  Falk  and  Pickle  are  from  the  Environmental  Epidemiology  Branch 
of  the  National  Cancer  Institute  in  Bethesda,  MD. 

Reprint  requests  should  be  sent  to  Pelayo  Correa,  MD,  Dept  of 
Pathology,  LSU  Medical  Center,  1901  Perdido  Street, 
New  Orleans,  LA  70012. 


JOURNAL  VOL  140  APRIL  49 


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with  our  Army  Medical  Person- 
nel Counselor. 


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LOOKING  FOR 
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LOUISIANA  TUMOR  REGISTRY 


JEAN  FIKE  CRAIG,  MS;  VIVIEN  W.  CHEN,  PhD; 
PELAYO  CORREA,  MD;  ELIZABETH  T.H.  FONTHAM,  DPH 


As  a population-based  registry^  the  Louisiana 
Tumor  Registry  (LTR)  provides  resources  to 
combat  the  serious  cancer  problem  in  Louisiana.  In 
1988  the  Registry  completed  its  expansion  and  now 
covers  the  state.  Using  a regional  registry  system, 
the  LTR  is  available  to  provide  research 
collaboration  as  well  as  assessments  of  the  cancer 
problem  in  the  state.  In  addition,  the  LTR  assists 
in  planning  health  care  services  for  a specific 
geographic  area  and  in  implementing  hospital 

tumor  registries. 


Abielatively  new  resource  for  cancer  prevention 
and  control  is  available  to  Louisiana's  health  care 
community  — a statewide  population-based  tumor 
registry. 

The  Louisiana  Tumor  Registry  (LTR)  was  first 
established  in  1974  by  Charity  Hospital  as  a popula- 
tion-based registry  for  the  New  Orleans  area  and  as 
a participant  in  the  Surveillance,  Epidemiology  and 
End  Results  (SEER)  program  of  the  National  Cancer 
Institute  (NCI).  LTR  was  transferred  to  the  State  Of- 
fice of  Health  in  1979  as  a pilot  for  a statewide  registry; 
federal  funding  ceased  in  1980.  Presently,  LTR  is  op- 
erated under  the  Department  of  Health  and  Human 
Resources  (DHHR)  umbrella  in  the  Office  of  Preven- 
tive and  Public  Health  Services.  Funding  for  the  reg- 
istry is  provided  from  the  proceeds  of  a state  cigarette 
tax  dedicated  to  cancer  research.  Since  1983,  LTR  has 
gradually  expanded  region  by  region  until  coverage 
of  the  entire  state  was  achieved  in  1988. 

Policies  for  the  LTR  are  set  by  the  Louisiana  Can- 
cer and  Lung  Trust  Fund  Board.  The  11  members  of 
the  Board  represent  various  health  institutions  and 
are  appointed  by  the  governor.  The  operations  of  the  ► 

JOURNAL  VOL  140  APRIL  51 


registry  are  mandated  by  public  law,  RS  40:1299.80  et 
seq,  which  directs  hospitals  and  pathology  laborato- 
ries to  report  their  cancer  cases  to  the  registry  so  that 
the  frequency  of  cancer  in  the  state  can  be  monitored. 
This  same  law  mandates  strict  confidentiality  of  the 
data,  a requirement  meticulously  observed  by  LTR 
personnel.  In  the  14  years  of  operation,  not  a single 
incident  compromising  the  confidentiality  of  the  in- 
formation gathered  has  occurred.  The  law  also  grants 
to  all  participating  institutions  immunity  from  any 
liability  which  may  arise  from  their  reporting  of  cases 
to  the  registry. 

OPERATIONS 

In  order  to  compile  statistics  on  the  frequency  and 
types  of  cancer  within  defined  geographic  areas,  the 
LTR  collects  information  from  various  departments  of 
all  hospitals  in  those  areas,  including  medical  records, 
pathology,  radiology,  and  hematology.  In  addition, 
cases  are  identified  from  free-standing  pathology  lab- 
oratories and  radiation  centers,  one-day  surgery  fa- 
cilities, private  physicians'  offices,  coroners'  offices, 
and  the  state  mortality  file.  To  ensure  accuracy  in 
calculating  incidence  rates,  cancers  occurring  among 
residents  who  are  diagnosed  and/or  treated  outside 
the  geographic  area  are  also  included  and  all  duplicate 
reports  of  cases  are  collated  into  one  record.  Non- 
resident cases  are  excluded  in  incidence  computa- 
tions. 

In  order  to  have  an  efficient  statewide  popula- 
tion-based registry,  the  LTR  uses  a regional  registry 
system  to  collect  data  from  all  parishes.  The  regional 
tumor  registries  are:  Baton  Rouge  Regional  Tumor 
Registry,  Acadiana  Tumor  Registry,  Southwest  Lou- 
isiana Regional  Tumor  Registry,  Northeast  Louisiana 
Regional  Tumor  Registry,  Regional  Tumor  Registry 
for  Northwest  Louisiana,  and  the  Alexandria-area  Re- 
gional Tumor  Registry.  The  regional  registries  coor- 
dinate the  collection  of  cancer  data  on  residents  of 
their  own  regions  from  all  sources  and  submit  them 
to  the  central  office  in  New  Orleans.  They  are  re- 
sponsible for  performing  quality  control  in  their  re- 
gions and  ensuring  complete  coverage.  The  regional 
registries  also  provide  training  to  hospital  staff  and 
collect  follow-up  information. 

SERVICES  PROVIDED 

While  most  physicians  are  familiar  with  hospital-based 
52  JOURNAL  VOL  140  APRIL 


tumor  registries  and  the  services  they  offer,  many  are 
not  aware  of  the  role  of  population-based  tumor  reg- 
istries. 

The  primary  concern  of  a population-based  tu- 
mor registry  is  to  monitor  the  frequency  of  cancer  in 
the  community.  Services  provided  by  the  LTR  to  Lou- 
isiana residents  include: 

1.  Assessment  of  the  cancer  problem.  Age-specific 
and  age-adjusted  incidence  and  mortality  rates  are 
calculated  by  the  LTR  using  population  statistics  from 
the  Census  Bureau  along  with  incidence  data  and 
Louisiana  Vital  Statistics  information.  These  rates  can 
be  compared  with  national  rates  and  rates  of  other 
states  and  even  other  countries  to  assess  the  magni- 
tude of  the  cancer  problem  in  Louisiana.  In  addition, 
unusually  high-risk  or  low-risk  groups  and  geo- 
graphic clusters  of  cases  can  be  identified. 

As  a population-based  registry,  the  LTR  also 
monitors  trends  in  cancer  incidence  and  mortality. 
The  data  base  already  established  permits  detection 
of  changes  in  cancer  patterns  within  the  state  and  can 
be  used  to  assess  the  effectiveness  of  cancer  programs 
in  the  community.  For  example,  a shift  to  an  earlier 
stage  of  disease  at  diagnosis  may  be  the  result  of  a 
successful  screening  program  and  a decline  in  mor- 
tality may  reflect  advances  in  clinical  management. 

2.  Research  collaboration.  The  collaboration  of  a 
population-based  tumor  registry  has  been  a prereq- 
uisite for  many  NCI  epidemiologic  research  grants. 
The  LTR  is  a participant  in  an  on-going  epidemiologic 
study  of  black/white  differences  in  cancer  patient  sur- 
vival experience  conducted  by  Louisiana  State  Uni- 
versity Medical  School  in  collaboration  with  NCI.  In 
a recent  Louisiana  project,  the  LTR  has  collaborated 
with  a Lake  Charles  environmental  group,  CLEAN, 
to  investigate  cancer  in  Calcasieu  Parish.  As  a member 
of  the  International  Association  of  Cancer  Registries, 
the  LTR  participates  in  various  research  projects  and 
reports  its  rates  for  publication  in  Cancer  Incidence  in 
Five  Continents,  the  most  prestigious  publication  on 
cancer  incidence. 

3.  Other  services  and  requests.  Other  services  of  the 
LTR  are  provided  upon  request.  Cancer  statistics  and 
reports  using  aggregate  data  are  available  at  no  charge. 
When  identifying  data  are  requested,  the  LTR  serves 
only  as  an  intermediary,  notifying  the  hospital  of  the 
request  and  relaying  the  response  to  the  researcher. 
All  identifying  information,  including  hospital  and 


! physician,  are  confidential  and  procedures  to  ensure 
; confidentiality  are  strictly  maintained.  While  reports 
lean  be  prepared  comparing  one  hospital  to  the  rest 
! of  the  hospitals  in  a geographic  area,  only  data  from 
the  requesting  hospital  can  be  identified  separately, 
i Information  identifying  specific  hospitals  cannot  be 
released  to  other  facilities. 

The  LTR  has  library  resources  of  specialized  can- 
cer epidemiological  information.  It  also  offers  assist- 
ance by  suggesting  bibliographic  references  by  tele- 
phone. Speakers  are  available  to  discuss  cancer  in 
Louisiana:  its  epidemiology,  trends  and  comparisons 
with  the  national  rates.  Students  and  the  press,  as 
weU  as  physicians,  are  frequent  requestors  of  infor- 
mation on  cancer  in  Louisiana. 

In  addition,  the  LTR  provides  consultation  and 
assistance  in  the  plarming  and  implementation  of  both 
regional  and  hospital  tumor  registries.  It  also  assists 
in  planning  the  health  care  services  in  a specific  geo- 
graphic area.  By  utilizing  LTR-computerized  infor- 
mation, marketing  departments  of  hospitals  and  other 
health  care  institutions  can  determine  the  needs  and 
demands  for  utilizing  certain  equipment  or  facilities 
I for  cancer  patients. 

PUBLICATIONS  AND  HIGHLIGHTS 

The  LTR  publishes  numerous  reports  among  which 
are  Cancer  in  Louisiana  (published  annually)  and  data 
for  inclusion  in  Cancer  Incidence  in  Five  Continents.  A 
few  highlights  from  these  publicaitons  are  listed  be- 
low: 

• Excess  cancer  mortality  for  the  oral  cavity  and  lung 
has  been  observed  in  Louisiana  males  since  1930.^ 

• For  the  decade  of  the  70s,  Louisiana  ranked  first  in 
lung  cancer  mortality  among  white  males,  25% 
higher  than  the  national  rate.^ 

• During  the  period  1974-1977,  New  Orleans  white 
males  experienced  the  highest  risk  for  lung  cancer 
among  all  SEER  participants;  the  incidence  rate  was 
40%  higher  than  the  SEER  rate.^ 

• New  Orleans  black  males  have  the  highest  inci- 
dence rate  for  lung  cancer  ever  reported  world- 
wide.^ 

• White  females  in  Louisiana  were  foimd  to  have  lower 
mortality  rates  for  most  cancer  sites  when  compared 
to  the  national  averages.  Similarly,  lower  incidence 
rates  for  most  cancers  were  observed  for  white  fe- 
males in  metropolitan  New  Orleans.^- ^ 


• White  females  in  New  Orleans  had  the  lowest  in- 
cidence rate  for  cancer  of  the  uterine  corpus  in  the 
country  — about  half  the  national  average.^ 

• Lung  cancer  surpassed  breast  cancer  to  become  the 
leading  cause  of  cancer  death  for  Louisiana  white 
women  in  1980,  six  years  prior  to  the  predicted  time 
for  the  nation.^ 

• A marked  decrease  in  mortality  for  Hodgkin's  dis- 
ease was  observed  from  1974  to  1981  while  inci- 
dence remained  stable.  This  strongly  suggests  im- 
provement in  survival  resulting  from  advances  in 
clinical  management  — a positive  impact  on  the 
health  of  the  Louisiana  population.^ 

• Age-specific  mortality  for  cancers  of  the  oral  cavity 
and  pharynx,  esophagus,  and  larynx  exhibited  a 2- 
slope  curve.  This  apparently  indicates  either  a non- 
homogeneous  delivery  of  carcinogens  over  time  or 
an  increase  in  incidence  in  younger  cohorts  by  the 
introduction  of  a new  carcinogen  or  an  increase  in 
the  dose  of  an  old  one.^ 

• Pre-menopausal  peaks  were  found  in  both  age-spe- 
cific incidence  and  mortality  curves  for  cervical  can- 
cer in  both  white  and  black  Louisiana  women,  sug- 
gesting a new  emerging  epidemiologic  pattern  for 
this  disease.^' ^ 

• Atypical  mortality  curves  which  were  observed  for 
cancers  of  the  ovary,  bladder,  kidney,  and  multiple 
myeloma  need  further  research.^ 

CONCLUSIONS 

These  observations  represent  only  a fraction  of  the 
new  information  which  has  become  available  in  Lou- 
isiana through  the  LTR.  It  is  hoped  that  this  wealth 
of  information  will  be  increasingly  utilized  by  our 
health  professionals  for  a better  understanding  of  our 
cancer  problem  and  for  a concerted  effort  to  meet  the 
allenge  of  our  considerable  cancer  burden.  The  con- 
tribution of  the  LTR  to  cancer  research  and  control  is 
a tribute  to  the  Louisiana  physicians  who  have  made 
it  possible.  The  LTR  is  a resource  for  those  who  are 
concerned  about  cancer  in  Louisiana.  ■ 

To  obtain  services  or  to  receive  a copy  of  Cancer  in 
Louisiana,  please  write  to  Jean  Craig,  Director,  Louisiana 
Tumor  Registry,  PO  Box  60630,  New  Orleans,  LA  70160. 

REFERENCES 

1.  Correa  P,  Chen  VW,  Craig  JF,  et  al:  Cancer  in  Louisiana.  Baton  Rouge,  La, 
Louisiana  Division  of  Administration,  1984. 


JOURNAL  VOL  140  APRIL  53 


2.  Correa  P,  Chen  VW,  Craig  JF,  et  al:  Cancer  in  Louisiana,  vol  2.  Baton  Rouge, 
La,  Louisiana  Division  of  Administration,  1985. 

3.  Young  JL,  Perq^  CL,  Asire  AT:  Surveillance,  Epidemiology  and  End  Results: 
Incidence  and  Mortality  Data  1973-1977.  National  Cancer  Institute  publi- 
cation No.  81-2330.  Dept  of  Health  and  Human  Resources,  1981. 

4.  Waterhouse  J,  Muir  C,  Shanmugaratnam  K,  et  al:  Cancer  Incidence  in  Five 
Continents,  vol  4,  publication  No.  42.  Lyon,  France,  International  Agency 
for  Research  on  Cancer,  1982,  671-789. 

5.  Correa  P,  Chen  VW,  Craig  JF,  et  al:  Cancer  in  Louisiana,  vol  3.  Baton  Rouge, 
La,  Louisiana  State  University  Graphic  Services,  1986. 

6.  Chen  V,  Craig  JF,  Correa  P,  et  al:  Cancer  in  Louisiana,  vol  4.  Baton  Rouge, 
La,  Louisiana  State  University  Graphic  Services,  1987. 


Ms  Craig  is  director  of  the  Louisiana  Tumor  Registry,  Dept  of  Health 
and  Human  Resources  Office  of  Preventive  and  Public  Health  Services 

in  New  Orleans. 

Drs  Chen,  Correa,  and  Fontham  are  from  the  Dept  of  Pathology  at 
Louisiana  State  University  Medical  Center  in  New  Orleans. 

Reprint  requests  should  he  sent  to  Jean  F.  Craig,  Louisiana  Tumor 
Registry,  PO  Box  60630,  Room  305,  New  Orleans,  LA  70160. 


Dx:  recurrent 


EASI  HlOH  SI 


herpes  labialis 

“HERPECIN-L  is  my  treatment  of  choice  for 
perioral  herpes.”  GP,  NY 

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blisters  . . . used  soon  enough.”  DOS,  MN 

“HERPECIN-L^.  . . a conservative  approach 
with  lovir  risk/high  benefits.”  MD,  FL 

“Used  at  prodromal  symptoms  . . . blisters 
never  formed  . . . remarkable.”  DH,  MA 

“(Irt  clinical  trials) . . . response  was  dramatic. 
HERPECIN-L  . .proven  far  superior.”  DOS,  PA 

“All  patients  claimed  shorter  duration  ...  at 
prodromal  symptoms  . . . HERPECIN  L 
averted  the  attacks.”  MD,  AK 


OTC.  See  P.D.R.  for  information.  For  samples  to  make 
your  own  clinical  evaluation,  write;  Campbell  Laboratories, 
Inc..  P.O.  BOX  812*MD,  FDR  STATION,  NEW  YORK,  N.Y. 
10150 


In  Louisiana  HERPECIN-L  is  available  at  all  Eckerd, 
K & B and  Walgreens  and  other  select  pharmacies. 


LOUISIANA  CANCER  AND  LUNG 
TRUST  FUND  BOARD 


ELECK  CRAIG,  MS;  CHARLES  L.  BROWN  JR,  MD 


The  Louisiana  Cancer  and  Lung  Trust  Fund  Board, 
which  was  established  in  1980,  encourages  research 
on  Louisiana's  cancer  problem  by  awarding  grants 
on  topics  related  to  cancer  in  Louisiana.  Support 
for  the  research  and  for  the  Louisiana  Tumor 
Registry,  which  is  supervised  by  the  Louisiana 
Cancer  and  Lung  Trust  Fund  Board,  is  provided  by 
funding  from  a dedicated  cigarette  tax.  Titles  of 
funded  applications  are  listed  along  with  a brief 
description  of  the  Louisiana  Cancer  Consortium 
which  was  also  established  through  the  efforts  of 
the  Louisiana  Cancer  and  Lung  Trust  Fund  Board. 

The  need  for  additional  funding  for  cancer 
research  to  combat  the  serious  cancer  burden  in 

Louisiana  is  emphasized. 


The  Louisiana  Cancer  and  Lung  Trust  Fund  Board 
was  created  in  1980  by  Legislative  Act  825  and  was 
administratively  placed  within  the  Department  of 
Health  and  Human  Resources.  The  Board  has  two 
major  mandates  from  the  state  legislature:  to  oversee 
the  Louisiana  Tumor  Registry,  a population-based 
registry  providing  data  on  the  incidence  of  cancer  in 
the  state;  and  to  encourage,  through  the  awarding  of 
grants,  research  on  the  cancer  problem  in  Louisiana. 

FUNDING 

Since  1984,  the  Louisiana  Cancer  and  Lung  Trust  Fund 
Board  has  received  1 million  dollars  per  year  in  ded- 
icated tobacco  taxes.  In  addition,  the  Board  is  au- 
thorized to  receive  contributions  for  cancer  research. 

ORGANIZATIONAL  STRUCTURE 

Officers  of  the  Board  include  a chairman,  vice-chair- 
man, and  secretary-treasurer.  There  are  four  active 
committees:  Budget,  Tumor  Registry,  Research,  and 
Advisory.  The  Board  meets  a minimum  of  three  times 
a year.  Members  do  not  receive  any  compensation  for  ► 

JOURNAL  VOL  140  APRIL  55 


their  services  and  are  entitled  only  to  reimbursement 
for  travel  expenses. 

BOARD  MEMBERSHIP 

The  members  of  the  Board  representing  eleven  insti- 
tutions are  appointed  by  the  governor.  Current  mem- 
bers of  the  Board  and  the  organizations  they  represent 
are: 

Charles  L.  Brown  Jr,  MD,  chairman,  New  Orleans 
(representing  American  Cancer  Society) 

George  H.  Porter  III,  MD,  vice-chairman,  New  Orleans 
(representing  Alton  Ochsner  Medical  Foundation) 
Andrew  S.  Ranier,  MD,  secretary-treasurer.  Lake 
Charles 

(representing  Louisiana  State  Medical  Society) 
Lawrence  S.  Baum,  PhD,  Monroe 
(representing  American  Lung  Association) 

R.  Davilene  Carter,  MD,  Metairie 
(representing  Tulane  Medical  School) 

Pelayo  Correa,  MD,  New  Orleans 
(representing  LSU  Medical  Center-New  Orleans) 

Carl  G.  Kardinal,  MD,  New  Orleans 
(representing  Leukemia  Society  of  Louisiana) 

Michael  H.  Martin,  MBA,  Baton  Rouge 
(representing  Perkins  Radiation  Center) 

John  M.  Rainey,  MD,  Lafayette 

(representing  Acadiana  Medical  Research  Foundation) 
George  J.  Thomas  Jr,  MD,  New  Orleans 
(representing  Flint-Goodridge  Hospital) 

Darryl  M.  Williams,  MD,  Shreveport 
(representing  LSU  Medical  Center-Shreveport) 

PROGRESS 

The  establishment  of  a statewide  tumor  registry,  as 
mandated  by  the  legislature,  has  been  pursued  by  a 
step-wise  coverage  of  the  state  initiated  in  the  New 
Orleans  metropolitan  area  and  completed  in  1988  with 
the  coverage  of  the  Alexandria  area.  A state  tumor 
registry  provides  information  on  incidence,  mortality, 
and  survival  of  cancer  patients.  These  data  are  the 
basic  building  blocks  for  research  in  cancer  epide- 
miology and  for  designing  strategies  of  cancer  control 
in  the  state. 

The  second  mandate  was  to  fund  research  proj- 
ects. In  the  last  three  years,  the  Board  has  funded  the 
following  22  research  projects  related  to  cancer  in  Lou- 
isiana: 


Comparison  of  nutrient,  pesticide,  and  mineral  removal  in 
home  tap  filters 

Detoxification  of  chemically  contaminated  drinking  water 
Screening  for  carcinogenic  exposures  in  exfoliated  human 
cells 

Conference  on  the  use  of  aquatic  animals  as  indicators  of 
environmental  pollution 

Occurrence  of  the  carcinogen  safrole  in  Louisiana's  food 
Chromosomal  aberrations  and  neoplastic  disposition 
Transplacental  tobacco  exposures 
Heredity  of  lung  cancer  in  Acadians 
Cancer  rates  in  Mississippi  River  catfish:  A pilot  study 
Racial  differences  in  the  prognosis  of  cancer  of  uterine  corpus 
Risk  factors  of  cancer  of  the  uterine  corpus  in  New  Orleans 
The  role  of  genetic  predisposition  in  childhood  neoplasia 
Worksite  smoking  control,  discouragement,  and  cessation 
Carcinogens  in  rural  groundwater  and  human  blood 
Risk  assessment  for  trihalomethanes  in  northeast  Louisiana 
Volatile  synthetic  organics  in  mother's  milk 
Lung  cancer  in  non-smoking  women,  radon  exposure 
A comparison  of  treatment  strategies  for  smoking  cessation 
Pilot  of  a school-based  smoking  prevention  program  for  ninth 
graders 

Immunopathogenesis  of  bronchogenic  carcinoma  in  Loui- 
siana asbestos-exposed  population 

Summaries  of  completed  research  projects  funded  by 
the  board  are  included  in  Cancer  in  Louisiana  published 
annually  by  the  Louisiana  Tumor  Registry. 

In  1985  the  Board  funded  the  Louisiana  Cancer 
Consortium.  The  aim  of  the  Consortium,  as  envi- 
sioned by  the  Board,  was  to  bring  all  academic  insti- 
tutions into  one  group  to  plan  and  develop  cancer 
control  research  activities  which  would  be  eligible  for 
federal  funding.  The  Consortium  would  in  effect  be 
a cancer  research  center  without  walls.  Members  of 
the  Consortium  include:  Louisiana  State  University 
Medical  School-New  Orleans,  Louisiana  State  Uni- 
versity Medical  School-Shreveport,  Tulane  University 
School  of  Medicine,  Tulane  School  of  Public  Health 
and  Tropical  Medicine,  Alton  Ochsner  Medical  Foun- 
dation, and  the  Department  of  Health  and  Human 
Resources.  After  three  years  of  funding  by  the  Board, 
the  future  of  the  Louisiana  Cancer  Consortium  ap- 
pears assured  as  it  has  been  incorporated  as  a non- 
profit organization  and  the  member  organizations  have 
agreed  to  assume  financial  responsibility  for  a full- 
time director.  The  Consortium  has  begun  several  col- 
laborative pilot  projects  including  a survey  of  re- 


56  JOURNAL  VOL  140  APRIL 


BOOKS  RECEIVED 


I 


sources  for  cancer  in  Louisiana  and  has  gained  sup- 
port from  major  cancer  institutions  and  schools  in  the 
state. 

! FUTURE  PLANS 

The  total  projected  cost  of  the  research  applications 
received  by  the  Board  in  the  last  three  years  was 
$3,298,222,  but  only  $577,045  was  available  for  re- 
search. Many  peer-approved  applications  are  going 
unfunded.  The  price  of  scientific  research  is  high,  but 
it  must  be  continued.  Even  though  Louisiana  has  a 
high  cancer  rate,  it  does  not  receive  its  share  of  federal 
resources  to  investigate  or  combat  the  problem.  By 
awarding  seed  money  to  investigators  for  research, 
Louisiana  will  attract  both  scientists  and  federal  fund- 
I ing  for  future  research. 

I Now  that  the  Board  has  completed  the  tumor 
registry  expansion,  cancer  statistics  will  be  available 
to  be  used  for  cancer  research  activities  statewide. 
Using  the  information  gathered,  analytic  studies  are 
I being  planned  to  address  the  cancer  problem  in  Lou- 
isiana. New  operating  funds  will  be  required  to  im- 
plement a new  data  storage  system.  This  system  is 
necessary  to  allow  us  to  interact  with  similar  computer 
systems  throughout  the  United  States. 

An  effort  will  be  made  to  continue  acquiring  mon- 
ies, from  private  and  governmental  sources,  for  the 
Board's  many  activities.  The  monies  available  need  to 
be  increased  by  at  least  100%  in  order  to  fully  carry 
out  the  mission  of  the  Board.  ■ 

For  additional  information,  please  contact  Dr  Charles 
L.  Brown  Jr,  Chairman,  200  West  Esplanade,  Kenner,  LA 
70065,  (504)  464-8600  or  Mr  Eleck  Craig,  Administrator, 
PO  Box  60630,  New  Orleans,  LA  70160,  (504)  568-2606. 


Mr  Craig  is  administrator  of  the  Louisiana  Cancer  and  Lung  Trust 
Fund,  Louisiana  Department  of  Health  and  Human  Resources,  Office  of 
Preventive  and  Public  Health  Services  in  New  Orleans. 

Dr  Brown  is  chairman  of  the  Louisiana  Cancer  and  Lung  Trust  Fund 
Board.  He  is  also  a clinical  professor  of  medicine  at  Tulane  University 
and  is  in  private  practice  at  the  Mahorner  Clinic  in  New  Orleans. 

Reprint  requests  should  be  sent  to  Eleck  Craig,  Louisiana  Cancer  and 

Lung  Trust  Fund,  PO  Box  60630, 
New  Orleans,  LA  70160. 


The  JOURNAL  seeks  reviews  of  the  following  books.  Interested 
physicians  should  contact  Frank  J.  Ilardi,  MD,  Book  Review  Editor, 
5000  Highway  190,  Suite  D-3,  Covington,  LA  70433. 

PRACTICAL  MICROSCOPIC  HEMATOLOGY: 

A MANUAL  FOR  THE  CLINICAL  LABORATORY 
AND  CLINICAL  PRACTICE 

Fritz  Heckner,  MD,  H.  Peter  Lehmann,  PhD,  Yuan  S.  Kao, 
MD;  Baltimore,  Urban  & Schwarzenberg  Inc,  1988,  97  pages. 

CLINICAL  ELECTROCARDIOGRAPHY: 

A PRIMARY  CARE  APPROACH 

Ken  Grauer,  MD,  R.  Whitney  Curry,  Jr,  MD;  Oradell,  NJ, 
Medical  Economics  Books,  1987,  544  pages. 

OB/GYN  EMERGENCIES:  THE  FIRST  SIXTY  MINUTES 
Roy  Farrell,  MD  (ed);  Rockville,  MD,  Aspen  Publishers  Inc, 

1986,  340  pages. 

ENDOCERVICAL  CARCINOMA: 

A CERVICOSCOPIC  ATLAS 

Minoru  Ueki,  MD;  St  Louis,  Ishiyaku  Euroamerica  Inc,  1987, 
90  pages. 

THE  CLINICAL  GENETICS  HANDBOOK 

Ruth  Berini  (ed);  Oradell,  NJ,  Medical  Economics  Books,  1986, 
385  pages. 

INTERPRETING  CARDIAC  DYSRHYTHMIAS 

Marcus  Wharton,  MD,  Nora  Goldschlager,  MD;  Oradell,  NJ, 
Medical  Economics  Books,  1986,  241  pages. 

NEUROLOGY:  PROBLEMS  IN  PRIMARY  CARE 

James  L.  Bernat,  MD,  Frederick  M.  Vincent,  MD;  Oradell, 

NJ,  Medical  Economics  Books,  1987,  656  pages. 

INFORMED  CONSENT:  A SURVIVAL  GUIDE 

Donald  J.  Palmisano,  MD,  JD,  Hebert  J.  Mang  Jr,  JD;  New 

Orleans,  Invictus  Publishing  Co,  1987,  47  pages. 

TO  BE  OR  NOT  TO  BE  HUMAN: 

THE  TRAITS  OF  HUMAN  NATURE 

Ben  Freedman,  MD;  New  York,  Vantage  Press,  1987,  509 
pages. 

THE  AGE  OF  MIRACLES 

Guy  Williams;  Chicago,  Academy  Chicago  Publishers,  1987, 
221  pages. 

PRIMARY  CARE  OF  CANCER 

Edward  A.  Mortimer  Jr,  MD  (ed);  Cleveland,  Case  Western 
Reserve  University  School  of  Medicine,  1987,  190  pages. 

HEALING  INTO  LIFE  AND  DEATH 

Stephen  Levine;  Garden  City,  NY,  Anchor  Press/Doubleday, 

1987,  290  pages. 

SICKLE-CELL  ANEMIA  AND  THALASSEMIA 

Newfoundland,  Canada,  Canadian  Sickle-Cell  Society,  1987. 


JOURNAL  VOL  140  APRIL  57 


PROFESSIONAL  LISTINGS 


J 

t; 

f 

1 


THE  FERTILITY  INSTITUTE  OF  NEW  ORLEANS 

{A  Professional  Corporation) 

Richard  P.  Dickey,  MD,  PhD  Steven  N.  Taylor,  MD 

Diplomate,  American  Board  of  Diplomate,  American  Board  of 

Reproductive  Medicine  Obstetrics  and  Gynecology 

Diplomate,  American  Board  of 
Obstetrics  and  Gynecology 

David  N.  Curole,  MD  Phillip  H.  Rye,  MD  Terry  Olar,  PhD 

Diplomate,  American  Board  Diplomate,  American  Board  Director,  InVitro  Laboratory 

of  Obstetrics  and  Gynecology  of  Obstetrics  and  Gynecology  Member,  Society  for  the 

Study  of  Reproduction 

REFERRALS  ACCEPTED  FOR  IN  VITRO  FERTILIZATION 
AND  OTHER  INFERTILITY  THERAPY  INCLUDING: 

MICROSURGERY  AND  LASER-MICROSURGERY  OF  THE  INFERTILE  FEMALE 
MANAGEMENT  OF  RECURRENT  AND  THREATENED  ABORTIONS  THROUGH  THE  FIRST  TRIMESTER 
LABORATORY  FACILITIES  FOR  COMPLETE  ANDROLOGY  AND  ENDOCRINOLOGY  TESTING 
INCLUDING  OVUM  PENETRATION  (HAMSTER  EGG) 


MAIN  OFFICE 

SLIDELL  OFFICE 

UPTOWN  OFFICE 

6020  Bullard  Ave 
New  Orleans,  LA  70128 
(504)  246-8971 
(504)  246-8795 

700  Cause  Blvd 
Suite  101 
Slidell,  LA  70458 

2633  Napoleon  Ave 
Suite  805 

New  Orleans,  LA  70115 

TOURO  INFIRMARY'S  CENTER  FOR  CHRONIC  PAIN 

1401  Foucher  St 
New  Orleans,  LA  70115 
(504)  897-8404 

AND 

DISABILITY  REHABILITATION 

Richard  H.  Morse,  MD 

Medical  Director 

Jackie  Chauvet 

Liaison  Coordinator 

Elizabeth  Messina,  RN 

Unit  Supervisor 

58  JOURNAL  VOL  140  APRIL 


BwaiaaBrnniaiwiwwafliifli^ 


stages 


kiDrwffy 

UNIVERSITY  OF  MARYLAND 
BALTIMORE 

JUN  2 1988 


stacit^ 


Mca 


MOT  10  CIRC. 


JOURNAL 

OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY  May  1988 


VJ^ 


Louisiana 


Physicians 


Insurance  Agency,  INC. 

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Chairman,  CONWAY  S.  MAGEE,  MD 
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EMILE  K.  VENTRE  JR,  MD 
Ex  officio,  DANIEL  H.  JOHNSON  JR,  MD 

EDITORIAL  BOARD 

KENNETH  B.  FARRIS,  MD 
RODNEY  C.  JUNG,  MD 
CONWAY  S.  MAGEE,  MD 
W.  CHARLES  MILLER,  MD 
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PANEL  OF  CONSULTANTS 

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FRANK  J.  ILARDI,  MD 
HENRY  W.  JOLLY  JR,  MD 
TERRY  R.  JONES,  MD 
SHELDON  P.  KOTTLE,  MD 
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PAUL  B.  LANSING,  MD 
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ESTABLISHED  1844.  Owned  and  edited  by  The 
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I ou 


OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY 


1988 


VOLUME  140  / NUMBER  5 / MAY 


ARTICLES 


Special  issue:  Cholesterol  and  coronary  heart  disease 


C.  Pratap  Reddy,  MD 

20 

Cholesterol  and  coronary 
heart  disease 

James  W.  Cox  Jr,  MD 
C.  Pratap  Reddy,  MD 

23 

Cholesterol  and  coronary 
atherosclerosis 

Larry  J.  Leyster,  MD 
Bryan  Lucenta,  MD 

27 

Diagnosis  and  evaluation 
of  hypercholesterolemia 

Alfredo  Lopez-S,  MD,  PhD 
Barbara  Y.  Legardeur,  MPH 

35 

New  guidelines  for  the 
treatment  of 
hyperlipidemia  in  adults 

Barbara  Y.  Legardeur,  MPH 
Alfredo  Lopez-S,  MD,  PhD 

39 

Dietary  treatment  of 
elevated  serum  cholesterol 

Steven  N.  Levine,  MD 

47 

Pharmacologic  treatment  of 
hypercholesterolemia 

DEPARTMENTS 

2 

Information  for  Authors 

15 

Auxiliary  Report 

3 

New  Members 

16 

Books  Received 

5 

ECG  of  the  Month 

19 

Calendar 

11 

Otolaryngology/Head 
& Neck  Surgery  Report 

59 

Classified  Advertising 

Cover  illustration  by  Eugene  New,  New  Orleans. 

INFORMATION  FOR  AUTHORS 


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jOURNALS 

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use  during  surgery.  Am  I Clin  Pathol  1979;71:680-692. 

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tion in  Cardiovascular  Medicine,  ed  2,  Smith  JT  (ed).  New 
York,  McCraw  Hill  Co,  1986,  pp  23-37. 

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NEW  MEMBERS 


Applications  for  membership  have  been  re- 
ceived from  the  following  physicians  by  the 
respective  parish  medical  societies  as  of 
Februarv  4,  1988.  The  Louisiana  State  Med- 
ical Society  is  pleased  to  welcome: 

■ Allen 

Chemparathy  V,  Manuel,  MD 

809  East  Seventh  Ave,  Oakdale  71463 
1978,  Nalanda  Medical  College,  India 
internal  medicine 

■ Calcasieu 

Stephen  L.  Carter  II,  MD 

2903  First  Ave,  Lake  Charles  70602 

1980,  LSU  School  of  Medicine,  New  Orleans 

pediatrics 

William  A.  Ross,  MD 

1801  Oak  Park,  Lake  Charles  70601 

1982,  University  of  California  College  of 
Medicine,  Irvine 

internal  medicine 

■ Jefferson  Davis 

Martha  S.  Edwards,  MD 

1207  S Lake  Arthur  Ave,  Jennings  70546 

1983,  LSU  School  of  Medicine,  New  Orleans 
internal  medicine 

■ Orleans 

Janet  D.  Barnes,  MD 

4335  Elysian  Fields,  Suite  203,  New  Orleans 
70122 

1978,  LSU  School  of  Medicine,  New  Orleans 
pediatrics 


Mark  G.  Ewell,  MD 

1430  Tulane  Ave,  Dept  of  Anesthesiology, 
New  Orleans  70112 

1983,  Texas  Tech  University  School  of  Med- 
icine, Lubbock 

anesthesiology 

Emile  J.  Labranche  III,  MD 

9930  Lake  Forest  Blvd,  New  Orleans  70127 

1984,  LSU  School  of  Medicine,  New  Orleans 
family  practice 

Sofjam  Lamid,  MD 

1542  Tulane  Ave,  New  Orleans,  LA  70112 
1960,  Faculty  of  Medicine  University  of  In- 
donesia, Indonesia 
physical  medicine  & rehabilitation 

Ira.  P.  Markowitz,  MD 

3600  Prytania,  Suite  71,  New  Orleans  70130 
1981,  Medical  College  of  South  Carolina, 
Charleston 
vascular  surgery 

Mary  Beth  Murnane,  MD 

2030  Whitney,  New  Orleans  70114 

1981,  LSU  School  of  Medicine,  New  Orleans 

pediatrics 

Glenda  J.  Richardson,  MD 

2222  Simon  Bolivar,  New  Orleans  70113 

1977,  LSU  School  of  Medicine,  New  Orleans 
pediatrics 

Ellis  E.  Williams,  MD 

4335  Elysian  Fields,  Suite  303,  New  Orleans 
70122 

1978,  University  of  Michigan  Medical  School, 
Ann  Arbor 

internal  medicine 


Robert  A.  Zimmerman,  MD 

2700  Napoleon  Ave,  New  Orleans  70113 
1983,  Tulane  University  School  of  Medicine, 
New  Orleans 
emergency  medicine 

■ Rapides 

Robin  R,  Bennett,  MD 

PO  Box  13030,  Alexandria  71315 

1978,  LSU  School  of  Medicine,  New  Orleans 

internal  medicine 

Wesley  W.  Davis,  MD 

405  Third  St,  Alexandria  71301 

1980,  LSU  School  of  Medicine,  Shreveport 

cardiology 

James  G.  Ralston,  MD 

65  Medical  Park  Blvd,  Suite  101,  PineviUe 
71360 

1982,  LSU  School  of  Medicine,  Shreveport 
ophthalmology 

Andrew  P.  Terry,  MD 

3311  Prescott  Rd,  Suite  200,  Alexandria  71301 

1983,  University  of  Alabama  School  of  Med- 
icine, Birmingham 

ophthalmology 

■ IntemI Resident  Members 

ORLEANS 

James  T.  LeMay,  MD 

1542  Tulane  Ave,  New  Orleans  70112 
1972,  University  of  Mississippi  School  of 
Medicine,  Jackson 
psychiatry 


JOURNAL  VOL  140  MAY  3 


Edouard  C.  (Ed)  Carrere,  Jr. 
attended  St.  Stanislaus 
from  1934-1939.  He  went 
on  to  become  a partner  in 
Ernest  A.  Carrere  s Sons  in 
New  Orleans  and  has  served 
on  the  Board  of  Directors  of  the 

American  Red  Cross,  the  Presidents  Council 
of  Loyola  University,  and  as  President  of  the 
Real  Estate  Commission  of  New  Orleans. 
“The  virtues  of  honesty  and  integrity  instilled 
in  me  at  St.  Stanislaus  were  the  trademark 
of  my  business.  My  word  is  my  bond” 

To  the  Brothers  of  the  Sacred  Heart, 
every  student  is  a potential  leader.  And  giving 
him  the  proper  example— spiritual,  intellectual 
and  moral  — is  our  mission  at  St.  Stanislaus. 

BOARDING  SCHOOL  GRADES  6-12 
SUMMER  CAMP  AGES  9-14 

304  South  Beach  Blvd.  Bay  St.  Louis,  MS  39520 

SAIIMT  STy\IMISI-ALJS 


St  Stanislaiis 
helps  build  leaders. 


FOR  A FREE  BROCHURE  CALL  THE  DIRECTOR  OF  ADMISSI0NS-(601)  467-9057. 


Norton  W.  Voorhies,  MD,  Editor 


ECG  OF  THE  MONTH 


MORE  THAN  MEETS  THE  EYE 

JORGE  I.  MARTINEZ-LOPEZ,  MD 


The  continuous  rhythm  strip  shown  below,  limb  lead  II,  was  recorded  on  a 58-year-old  man  with  severe 
chronic  obstructive  lung  disease. 


What  is  your  diagnosis?  Elucidation  is  on  page  7. 


JOURNAL  VOL  140  MAY  5 


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I 


ECG  Of  the  Month 

Case  presentation  is  on  page  5. 

DIAGNOSIS  — Sinus  rhythm;  atrial  parasystole 

The  most  obvious  finding  in  the  tracing  (courtesy  of 
Dr.  William  P.  Nelson)  is  the  presence  of  P waves 
with  two  different  morphologies:  one  is  broad  and 
notched;  the  other  is  tall  and  peaked.  The  broad  and 
notched  P waves  are  of  sinus  node  origin,  recur  at  a 
rate  of  65  times  a minute,  and  are  associated  with 
normal  PR,  QRS,  and  QT  intervals,  and  normal  ST 
segments  and  T waves. 

The  tall,  peaked  P waves,  on  the  other  hand,  are 
ectopic  and  their  positive  polarity  indicates  a high 
right  atrial  origin.  Ectopic  P waves  appear  frequently 
during  the  recording  — mostly  in  a trigeminal  pattern 
— at  rates  slower  than  the  sinus  rhythm,  and  are 
followed  by  QRS  complexes  that  are  either  similar  to 
or  broader  and  different  in  configuration  than  those 
of  the  sinus  rhythm,  and  by  normal  ST  segments  and 
T waves. 

It  is  the  nature  of  these  ectopic  P waves  (EP)  that 
forms  the  basis  for  the  discussion  to  follow. 

DISCUSSION 

It  would  be  very  easy  to  summarily  dismiss  the  ar- 
rhythmia shown  in  the  tracing  as  the  result  of  atrial 
premature  impulses.  However,  careful  analysis  of  the 
rhythm  strip  reveals  more  than  meets  the  eye. 

Atrial  premature  impulses  usually  display  fixed 
coupling  intervals  because  they  are  dependent  on  the 
preceding  cycle.  In  contrast,  the  coupling  intervals 
between  EPs  and  sinus  Ps  in  the  tracing  are  variable: 
some  EPs  occur  late  in  diastole,  while  others  occur  in 
early  or  mid-diastole.  Even  though  the  coupling  in- 
tervals are  variable,  intervals  between  consecutive  EPs 
(interectopic  intervals)  are  relatively  constant  except 
in  the  middle  panel,  where  the  first  EP-to-EP  interval 
is  longer  than  the  preceding  and  the  following  inter- 
ectopic intervals.  Lastly,  all  but  two  of  the  EP-to-sinus 
P intervals  (the  returning  cycles)  are  longer  than  the 
sinus  cycles;  the  two  that  are  not  are  about  equal  to 
the  sinus  cycles. 

The  combination  of  EPs  associated  with  variable 
coupling  intervals  and  with  interectopic  intervals  that 
are  either  equal  to  or  close  multiples  of  a common 
denominator  should  prompt  the  interpreter  to  con- 


sider the  ECG  diagnosis  of  atrial  parasystole. 

At  this  time,  it  is  important  to  present  briefly  the 
concept  of  parasystole.  Normally,  depolarization  of 
the  heart  is  initiated  and  dominated  by  impulses  gen- 
erated by  the  sinus  node.  Dual  cardiac  rhythms  can 
occur  when  two  separate  pacemakers  are  concur- 
rently in  operation,  eg,  complete  AV  block  and  other 
forms  of  AV  dissociation  and  parasystole. 

The  term  parasystole  (from  the  Greek,  beating  side- 
by-side)  designates  a group  of  arrhythmias  in  which 
there  is  "dual  activation  of  a single  cardiac  chamber 
in  which  one  pacemaker  (the  parasysfoHc  one)  is  pro- 
tected intermittently  or  totally  from  discharge  by  the 
prevailing  rhythm."  The  parasystolic  focus  (PF)  has 
special  characteristics.  First,  it  is  ectopic  and  may  be 
located  an5nvhere  in  the  heart.  Most  commonly,  PF 
is  located  in  the  ventricles,  less  commonly  in  the  AV 
node,  and  rarely  in  the  atria;  other  reported  sites  in- 
clude the  bundle  of  His  and  accessory  cardiac  path- 
ways. Second,  PF  is  an  independent  automatic  center 
of  impulse  formation  with  two  other  characteristics: 
entrance  and  exit  block.  Entrance  block  protects  PF  from 
extinction  by  advancing  electrical  fronts  that  other- 
wise would  invade  its  domain,  discharging  and  sup- 
pressing it.  As  a result,  PF  can  fire  regularly,  undis- 
turbed by  other  electrical  impulses.  Exit  block,  on  the 
other  hand,  occurs  in  the  opposite  direction  of  en- 
trance block  and  confines  the  ectopic  impulse  to  PF. 
The  degree  of  exit  block  exhibited  by  PF  will  deter- 
mine the  observed  manifest  rate. 

The  exact  location  of  PF  in  atrial  parasystole  is 
not  known;  a location  within  a major  atrial  prefer- 
ential conduction  pathway  in  the  right  atrium  has 
been  proposed.  When  an  atrial  PF  and  sinus  rhythm 
coexist,  both  compete  to  activate  the  atria  and  ven- 
tricles; the  focus  with  the  faster  rate  of  firing  will  be 
the  dominant  pacemaker  of  the  heart.  Manifest  rates 
of  between  20  and  375  a minute  have  been  reported 
in  atrial  parasystole,  but  rates  of  40  or  less  are  more 
common. 

Although  atrial  parasystole  is  not  abolished  by 
sinus  impulses,  maneuvers  that  transiently  increase 
vagal  tone,  as  well  as  mild  exercise  or  isoproterenol, 
may  terminate  atrial  parasystole.  Conversely,  the  sinus 
node  is  not  protected  from  atrial  parasystolic  impulses 
and  may  be  discharged  and  reset  by  them.  A variety 
of  factors  determine  whether  or  not  the  sinus  node 
will  be  discharged  and  reset  by  atrial  parasystolic  im- 
pulses. 


JOURNAL  VOL  140  MAY  7 


The  variation  in  the  morphology  of  the  QRS  com- 
plexes that  follow  EPs  in  the  tracing  is  attributed  to 
the  degree  of  refractoriness  encountered  downgrade 
by  the  advancing  ectopic  electrical  impulses:  narrow 
QRS  complexes  denote  normal,  and  wide  QRS  com- 
plexes aberrant,  ventricular  conduction. 

In  general,  treatment  of  atrial  parasystole  is  not 
required  because  the  arrhythmia  is  benign  and  usu- 
ally produces  neither  cardiac  symptoms  nor  hemo- 
dynamic changes.  In  most  instances,  reassurance  of 
the  patient,  the  use  of  sedatives  — if  the  patient  is 
apprehensive  — and  management  of  the  underlying 
cardiac  disease  is  all  that  is  necessary.  The  patient 
whose  tracing  is  shown  here  had  repetitive  episodes 
of  atrial  parasystole  for  at  least  three  years,  but  at  no 
time  did  he  have  episodes  of  triggered  atrial  activity. 
Once  during  the  three-year  period,  oral  quinidine  was 
given;  it  failed  to  suppress  the  arrhythmia,  but  pro- 
voked a devastating  diarrhea. 

Atrial  parasystole  goes  unrecognized  frequently 
because  it  is  a rare  cardiac  arrhythmia  and  because 
many  physicians  are  not  familiar  with  it  and  will  er- 
roneously identify  the  ectopic  P waves  as  atrial  pre- 
mature impulses.  Because  the  12-lead  ECG  is  not  of 
sufficient  length  to  raise  the  index  of  suspicion,  a long 
rhythm  strip  is  desirable  and  will  show  more  than 
meets  the  eye.  ■ 


SELECTED  REFERENCES 

1.  Langendorf  R,  Lesser  ME,  Plotkin  P,  et  al:  Atrial  parasystole  with  inter- 
polation. Am  Heart  J 1962;63:649-658. 

2.  Flowers  NC,  Copeland  GD,  Brody  DA:  Two  cases  of  supraventricular 
parasystole.  Circulation  1964;29:440-446. 

3.  Eliakim  M:  Atrial  parasystole:  Effects  of  carotid  sinus  stimulation,  Valsalva 
maneuver  and  exercise.  Am  J Cardiol  1965;16:457-461. 

4.  Friedberg  HD,  Schamroth  L:  Atrial  parasystole.  Br  Heart  J 1970;32:172- 
180. 

5.  Pick  A,  Langendorf  R:  Parasystole  and  its  variants.  Med  Clin  North  Am 
1976;60:125-147. 


Dr.  Martinez-Lopez  is  a specialist  in  cardiovascular  diseases  affiliated 
with  the  Cardiology  Service,  Dept  of  Medicine  at  William  Beaumont 
Army  Medical  Center  in  El  Paso,  TX. 

The  opinions  and  assertions  contained  herein  are  the  private  views  of  the 
author  and  not  to  he  construed  as  official  or  as  reflecting  the  views  of 
the  Dept  of  the  Army  or  Dept  of  Defense. 


ARAFATE" 

^(sucralfate)  Tablets 


BRIEF  SUMMARY 

CONTRAINDICATIONS 

There  are  no  known  contraindications  to  the  use  of  sucralfate. 

PRECAUTIONS 

Duodenal  ulcer  is  a chronic,  recurrent  disease.  While  short-term  treatment  with  sucralfate 
can  result  in  complete  healing  of  the  ulcer,  a successful  course  of  treatment  with 
sucralfate  should  not  be  expected  to  alter  the  post-healing  frequency  or  severity  of 
duodenal  ulceration. 

Drug  Interactions:  Animal  studies  have  shown  that  simultaneous  administration 
of  CARAFATE  (sucralfate)  with  tetracycline,  phenytoin,  digoxin,  or  cimetidine  will  result 
in  a statistically  significant  reduction  in  the  bioavailability  of  these  agents.  The  bioavailability 
of  these  agents  may  be  restored  simply  by  separating  the  administration  of  these 
agents  from  that  of  CARAFATE  by  two  hours.  This  interaction  appears  to  be  nonsys- 
temic  in  origin,  presumably  resulting  from  these  agents  being  bound  by  CARAFATE  in 
the  gastrointestinal  tract.  The  clinical  significance  of  these  animal  studies  is  yet  to  be 
defined.  Howevei;  because  of  the  potential  of  CARAFATE  to  alter  the  absorption  of 
some  drugs  from  the  gastrointestinal  tract,  the  separate  administration  of  CARAFATE 
from  that  of  other  agents  should  be  considered  when  alterations  in  bioavailability  are  felt 
to  be  critical  for  concomitantly  administered  drugs. 

Carcinogenesis,  Mutagenesis,  Impairment  of  Fertility:  Chronic  oral  toxicity 
studies  of  24  months'  duration  were  conducted  in  mice  and  rats  at  doses  up  to  1 gm/kg 
(12  times  the  human  dose).  There  was  no  evidence  of  drug-related  tumorigenicity.  A 
reproduction  study  in  rats  at  doses  up  to  38  times  the  human  dose  did  not  reveal  any 
indication  of  fertility  impairment.  Mutagenicity  studies  were  not  conducted. 

Pregnancy:  Teratogenic  effects.  Pregnancy  Category  B.  Teratogenicity  studies 
have  been  performed  in  mice,  rats,  and  rabbits  at  doses  up  to  50  times  the  human  dose 
and  have  revealed  no  evidence  of  harm  to  the  fetus  due  to  sucralfate.  There  are, 
however,  no  adequate  and  well-controlled  studies  in  pregnant  women.  Because  animal 
reproduction  studies  are  not  always  predictive  of  human  response,  this  drug  should  be 
used  during  pregnancy  only  if  clearly  needed. 

Nursing  Mothers:  It  is  not  known  whether  this  drug  is  excreted  in  human  milk. 
Because  many  drugs  are  excreted  in  human  milk,  caution  should  be  exercised  when 
sucralfate  is  administered  to  a nursing  woman. 

Pediatric  Use:  Safety  and  effectiveness  in  children  have  not  been  established. 

ADVERSE  REACTIONS 

Adverse  reactions  to  sucralfate  in  clinical  trials  were  minor  and  only  rarely  led  to 
discontinuation  of  the  drug.  In  studies  involving  over  2,500  patients  treated  with  sucralfate, 
adverse  effects  were  reported  in  121  (4.7%). 

Constipation  was  the  most  frequent  complaint  (2.2%).  Other  adverse  effects,  reported 
ih  no  more  than  one  of  every  350  patients,  were  diarrhea,  nausea,  gastric  discomfort, 
indigestion,  dry  mouth,  rash,  pruritus,  back  pain,  dizziness,  sleepiness,  and  vertigo. 

OVERDOSAGE 

There  is  no  experience  in  humans  with  overdosage.  Acute  oral  toxicity  studies  in 
animals,  however  using  doses  up  to  1 2 gm/kg  body  weight,  could  not  find  a lethal  dose. 
Risks  associated  with  overdosage  should,  therefore,  be  minimal. 

DOSAGE  AND  ADMINISTRATION 

The  recommended  adult  oral  dosage  for  duodenal  ulcer  is  1 gm  four  times  a day  on 
an  empty  stomach. 

Antacids  may  be  prescribed  as  needed  for  relief  of  pain  but  should  not  be  taken 
within  one-half  hour  before  or  after  sucralfate. 

While  healing  with  sucralfate  may  occur  during  the  first  week  or  two,  treatment 
should  be  continued  for  4 to  8 weeks  unless  healing  has  been  demonstrated  by  x-ray  or 
endoscopic  examination. 

HOW  SUPPLIED 

CARAFATE  (sucralfate)  1-gm  tablets  are  supplied  in  bottles  of  100  (NDC  0088-1712-47) 
and  in  Unit  Dose  Identification  Paks  of  100  (NDC  0088-1712-49).  Light  pink  scored 
oblong  tablets  are  embossed  with  CARAFATE  on  one  side  and  1712  bracketed  by  Cs  on 
the  other.  Issued  1/87 

References: 

1.  Korman  MG,  Shaw  RG,  Hansky  J,  etal:  Gasfroenfero/ogy  80:1451-1453, 1981. 

2.  Korman  MG,  Hansky  J,  Merrett  AC,  etal:  D;g  D/s  Sc/ 27:71 2-71 5, 1982. 

3.  Brandstaetter  G,  Kratochvil  P:  Am  J Med  79  (suppi  2C):36-38, 1985. 

4.  Marks  IN,  Wright  JR  Gilinsky  NH,  et  al:  J Clin  Gastroenterol  8:419-423, 1986. 

5.  Lam  SK,  Hui  WM,  Lau  WY,  etal:  Gasfroenfero/ogy 92:1193-1201, 1987. 


Another  patient  benefit  product  from 

PHARMACEUTICAL  DIVISION 

MARION 

LABORATORIES.  INC 

KANSAS  CITT.  MO  64137 


082  5 A8 


8 JOURNAL  VOL  140  MAY 


OTOLARYNGOLOGY/ 

HEAD  & NECK  SURGERY  REPORT 


EVALUATION  OF  FACIAL  NERVE 

PARALYSIS 

J.  KEVIN  DUPLECHAIN,  MD;  PAUL  A.  BLAIR,  MD,  FACS 


Evaluation  of  facial  paralysis  is  a difficult 
problem.  We  present  a brief  case  presentation  of  a 
patient  who  developed  facial  paralysis  secondary 
to  a blow  on  the  head.  His  workup  and  eventual 
outcome  is  detailed.  This  allows  for  a broad 
review  of  different  causes  of  facial  nerve  paralysis, 
and  in  detail,  describes  current  diagnostic  studies 
that  help  in  determining  these  causes  and  eventual 

outcome. 


A 37-year-old  black  male  came  to  the  otolaryngol- 
ogy clinic  four  days  after  being  struck  on  the  left 
side  of  the  head  complaining  of  left-sided  facial  pa- 
ralysis. On  the  day  the  injury  occurred,  he  was  taken 
to  the  emergency  room  for  evaluation  because  he  was 
momentarily  unconscious.  Physical  examination,  plain 
skull  films,  and  computed  tomography  scan  of  the 
head  were  normal.  At  presentation  to  our  cUnic  com- 
plete left-sided  facial  paralysis  was  evident.  The  re- 
mainder of  his  examination  was  significant  only  for 
a left  middle  ear  effusion.  Computed  tomography 
scans  were  reviewed  without  evidence  of  a fracture. 
Nerve  excitability  testing  (NET)  using  the  Hilger  stim- 
ulator revealed  no  asymmetry.  Audiogram  demon- 
strated a mild  conductive  loss  in  the  left  ear  and  an 
absent  stapedius  reflex.  He  was  admitted  to  the  hos- 
pital, placed  on  intravenous  steroids,  and  underwent 
serial  nerve  excitability  testing.  On  the  fourth  hospital 
day,  a 1.5  milliamp  difference  was  noted  during  NET. 
Intravenous  steroids  were  continued,  and  two  days 
later  facial  function  began  to  return.  He  was  subse- 
quently discharged  and  follow-up  evaluation  revealed 
approximately  90%  return  of  facial  nerve  function. 


JOURNAL  VOL  140  MAY  11 


I 


DISCUSSION 

Facial  nerve  paralysis  can  be  a distressing  condition 
for  both  patient  and  physician.  Whether  the  etiology 
is  traumatic,  neoplastic,  or  idiopathic,  careful  evalu- 
ation of  nerve  function  is  essential.  Historical  points 
in  the  evaluation  include  a history  of  trauma  to  the 
head  and/or  face,  previous  episodes  of  facial  paralysis 
and  rapidity  of  onset  of  the  paralysis.  In  the  trau- 
matized patient,  acute  onset  of  paralysis  may  indicate 
complete  transection  of  the  nerve,  in  which  case  ex- 
ploration should  be  undertaken.  A slow  and  pro- 
gressive palsy  over  several  days  suggests  a stretch 
type  injury.  Delayed  onset  of  paralysis,  usually  greater 
than  three  weeks,  is  most  suspicious  for  a neoplastic 
process.  Idiopathic  facial  paralysis  (ie,  BelFs  palsy) 
may  present  with  a complete  and  sudden  onset  of 
paralysis  or  a slower  progressive  palsy,  with  prog- 
nosis for  recovery  worse  in  the  former. 

Recurrent  facial  paralysis  can  be  grouped  into 
ipsHateral,  alternating,  and  bilateral.  Ipsilateral  con- 
ditions are  associated  with  neoplastic  processes. 
Schwannomas  have  been  the  most  common  benign 
neoplasm  causing  unilateral  facial  paralysis.^  Schwan- 
nomas arise  with  equal  incidence  from  the  facial  and 
acoustic  nerves.  Alternating  recurrent  facial  paralysis 
occurs  approximately  12%  of  the  time  in  Bell's  palsy. 
Of  the  more  unusual  conditions  that  cause  alternating 
facial  paralysis,  Melkerson  Rosenthal  Syndrome  (MRS) 
is  the  most  common.  Other  characteristics  of  MRS 
include  recurrent  edema  of  the  lips,  face  and  eyelids, 
cheilitis,  and  a fissured  tongue. 

Bilateral  simultaneous  paralysis  can  be  a result  of 
neurologic  disease  such  as  Guillian  Barre  Syndrome, 
granulomatous  diseases  including  sarcoidosis,  or  other 
neoplastic  disorders  such  as  leukemia. 


ANATOMY  OF  THE  FACIAL  NERVE 

The  facial  nerve  (Fig)  originates  from  the  pons  and 
emerges  from  the  brainstem  with  the  nervous  inter- 
medius,  and  then  joins  the  acoustic  nerve  to  enter 
into  the  internal  auditory  canal.  Distal  to  this  point, 
the  nerve  enters  the  fallopian  canal  which  can  be  di- 
vided into  3 segments:  1)  labyrinthine  segment,  2) 
tympanic  or  horizontal  segment,  and  3)  mastoid  or 
vertical  segment.  The  labyrinthine  segment  of  the  fal- 
lopian canal  extends  from  the  fundus  of  the  internal 


Fig.  Anatomy  of  the  facial  nerve  through  the  tem- 
poral bone 


auditory  canal  to  just  distal  to  the  geniculate  ganglion. 
The  nerve  is  exquisitely  sensitive  to  injury  here  be- 
cause the  canal  is  very  narrow,  and  this  segment  of 
the  nerve  lacks  anastomosing  arterial  arcades.^ 

Three  nerves  originate  within  this  segment.  The 
greater  petrosal  nerve  sends  preganglionic  parasym- 
pathetic fibers  via  the  pteryogopalatine  ganglion  to 
supply  secretory  function  to  the  lacrimal  gland.  An 
inconsistent  external  petrosal  nerve  carries  sympa- 
thetic fibers  to  the  middle  meningeal  artery.  The  third 
branch  is  the  lesser  petrosal  nerve  which  supplies 
secretomotor  function  to  the  parotid  gland. 

The  facial  nerve  then  makes  an  abrupt  turn  (genu) 
within  the  temporal  bone  where  the  tympanic  or  hor- 
izontal position  begins.  Within  this  segment,  no 
branches  arise.  The  final  segment  of  the  nerve  within 
the  fallopian  canal  gives  rise  to  two  separate  branches 
which  subsequently  innervate  the  stapedius  muscle 
and  supply  taste  to  the  anterior  two-thirds  of  the 
tongue.  A thorough  understanding  of  facial  nerve 
anatomy  within  the  temporal  bone  is  essential  for 
electrodiagnostic,  topognostic  studies,  audiometric 
and  radiologic  evaluation. 

TOPOGNOSTIC  TEST 

Topognostic  tests  are  site  of  lesion  test.  Their  utili- 
zation is  based  on  the  various  branches  of  the  facial 


12  JOURNAL  VOL  140  MAY 


nerve  within  the  temporal  bone.  These  tests  include 
the  Schirmer  test,  submandibular  salivary  flow  test, 
stapedius  reflex,  and  electrogustometry.  These  tests 
are  commonly  utilized  in  the  patient  with  head  trauma 
resulting  in  facial  paralysis. 

The  Schirmer  test  is  a means  of  quantitating  lac- 
rimation.  Normal  results  suggest  an  intact  greater  pe- 
trosal nerve  which  supplies  the  lacrimal  gland.  The 
test  is  performed  by  placing  5 mm  precut  portions  of 
filter  paper  into  the  medial  third  of  the  lower  lid.  At 
three  minutes  the  test  is  terminated  and  a measure 
of  tear  flow  is  obtained.  By  comparing  the  ratio  of  the 
normal  to  the  abnormal  side,  the  likelihood  of  a nerve 
injury  in  the  labyrinthine  segment  of  the  facial  nerve 
can  be  predicted.^ 

Submandibular  salivary  flow  is  dependent  on  the 
integrity  of  the  chordae  tympani  which  arises  within 
mastoid  segment  of  the  fallopian  canal,  synapses  in 
the  submandibular  ganglion  and  then  innervates  the 
submandibular  gland.  Testing  consists  of  selectively 
cannulating  the  ducts  in  the  floor  of  the  mouth,  and 
the  measuring  salivary  flow  for  a specified  time  pe- 
riod. Results  are  abnormal  when  salivary  flow  on  the 
affected  side  is  25%  of  the  normal  side.^ 

Stapedius  reflex  evaluation  is  essential  to  any 
workup  in  a patient  with  facial  paralysis.  Its  absence 
indicates  loss  of  innervation  of  the  stapedius  muscle, 
whose  nerve  supply  arises  from  the  mastoid  segment 
of  the  facial  nerve.  Middle  ear  pathology  must  be 
excluded  if  this  test  is  to  be  valid.  Electrogustometry 
is  a means  of  stimulating  the  taste  receptors  within 
the  tongue  electrically  to  evaluate  chordae  tympani 
integrity.^  The  reliability  of  this  test  is  not  good  be- 
cause of  the  subjective  interpretation  of  taste  by  dif- 
ferent individuals. 

ELECTRODIAGNOSTIC  STUDIES 

Electroneurography,  the  general  term  for  diagnostic 
studies  of  nerve  dysfunction,  has  modernized  facial 
nerve  testing.  It  has  become  helpful  in  defining  in- 
dications for  surgical  exploration  of  the  temporal  bone 
in  trauma  cases,  as  well  as  predicting  outcome  of  non- 
surgically  treated  patients  with  facial  nerve  dysfunc- 
tion. 

Different  degrees  of  nerve  injury  can  occur.  Tem- 
poral bone  fractures  sometimes  result  in  complete 
transection  of  the  nerve,  whereas  in  idiopathic  facial 
paralysis,  edema  of  the  nerve  is  thought  to  be  the 
likely  mechanism  causing  paralysis.  Electroneurog- 
raphy can  help  distinguish  the  varying  types  of  in- 


TABLE 

SUNDERLAND  CLASSIFICATION  OF  NERVE  INJURIES 

Class  1 

Neuropraxic 

No  loss  of  Axonal  Continuity 
NET  symmetric 

Class  II 

Axontemetic 

Axonal  disruption  and  Wallerian 
degeneration  occur 
NET  asymmetric 

Class  III 

Neurotemetic 

Endoneurial  disruption  occurs 

Class  IV 

Neurotemetic 

Perineural  disruption  occurs 

Class  V 

Neurotemetic 

Epineural  disruption  occurs 

Note:  Class  III,  IV,  V injuries  allow  for  partial  recovery  and 
synkenisia. 

juries.  Sunderland  classified  nerve  injuries  into  five 
distinct  categories  (Table). ^ 

NET  is  the  most  basic  of  electroneurography.  It 
is  a minimal  stimulation  test  commonly  performed 
with  a Hilger  nerve  stimulator.  It  determines  minimal 
nerve  excitatory  thresholds  and  can  distinguish  neu- 
ropraxic  from  more  severe  lesions.  Testing  is  per- 
formed by  comparing  the  normal  to  the  abnormal  side 
by  stimulating  the  nerve  at  its  trunk  where  it  exits  the 
stylomastoid  foramen.  A difference  of  3.5  milliamps 
between  normal  and  abnormal  sides  signifies  pro- 
gressive degeneration  of  the  nerve  and  significant  in- 
jury. 

Electroneurography  is  a more  standardized  and 
objective  test.  It  is  classified  as  a maximal  or  supra- 
maximal stimulation  test  because  the  voltage  is  in- 
creased on  the  voltage  stimulator  until  maximal  facial 
motion  is  obtained.  A recorder  electrode  is  placed  on 
the  nasolabial  fold  and  records  muscle  twitches  caused 
by  the  electrical  current.  Multiple  stimulations  are 
performed,  and  an  average  amplitude  is  obtained. 
This  is  then  compared  to  the  normal  amplitudes  ob- 
tained on  the  nonparalyzed  side.  The  percentage  of 
the  nerve  that  has  undergone  degeneration  is  calcu- 
lated, and  90%  degeneration  implies  that  without  in- 
tervention surgically,  the  prognosis  is  poor  for  recov- 
ery.^ 

Electromyography  or  the  recording  of  muscle  po- 
tentials within  the  facial  musculature  becomes  im- 
portant when  visible  or  electrical  stimulation  cannot  ^ 


JOURNAL  VOL  140  MAY  13 


be  recorded  by  electroneurography.  Characteristic  re- 
sponses can  help  predict  outcome.  In  a delayed  eval- 
uation, approximately  four  to  six  weeks  post  paral- 
ysis, electromyography  may  demonstrate  polyphasic 
reinnervation  potentials  indicating  nerve  regenera- 
tion and  no  reason  to  alter  treatment.  However,  as 
early  as  14  days  post  onset  of  paralysis,  fibrillation 
potentials  may  be  present  indicating  early  nerve  de- 
generation. 

AUDIOLOGIC  AND  RADIOGRAPHIC 
EVALUATION 

Audiologic  evaluation  of  any  patient  with  facial  nerve 
paralysis  should  include  pure  tone  audiogram  and 
stapedius  reflex.  In  unknown  cases  of  facial  paralysis 
this  can  help  distinguish  neoplastic  from  idiopathic 
causes.  In  the  trauma  patient,  absence  of  a stapedius 
reflex  with  an  otherwise  normal  middle  ear,  indicates 
a lesion  in  the  temporal  bone.  This  is  especially  im- 
portant in  the  trauma  patient. 

Radiographic  evaluation  is  probably  best  per- 
formed utilizing  high  resolution  computed  tomogra- 
phy with  maximal  bone  enhancement.  Scans  should 
range  from  the  stylomastoid  foramen  to  the  petrous 
apex.  Axial  and  coronal  views  should  be  obtained. 
Pleuridirectional  tomograms  are  also  very  useful,  but 
used  less.  Lateral,  anteroposterior,  and  20°  oblique 
views  should  be  obtained,  along  with  internal  audi- 
tory canal  views,  a common  site  for  neoplastic  proc- 
esses. 

CONCLUSION 

The  patient  presented  sustained  a neuropraxic  injury 
to  the  facial  nerve  within  the  temporal  bone.  This  case 
demonstrates  the  most  basic  evaluation  of  a patient 


with  facial  nerve  dysfunction.  A key  point  in  his  his- 
tory was  that  the  palsy  occurred  four  days  post  trauma, 
significantly  limiting  the  types  of  injury  that  could 
have  occurred.  If  the  trauma  had  transected  the  nerve, 
paralysis  should  have  been  immediate.  Other  key 
points  such  as  symmetric  NET  initially,  and  then  a 
difference  of  only  1.5  milliamps  subsequently  indi- 
cates a Class  I or  II  injury.  Had  NET  been  greater  than 
3.5  milliamps,  electroneuronography  would  have  been 
indicated. 

In  cases  which  are  not  as  clearly  defined,  the 
entire  battery  of  topognostic  and  electrodiagnostic 
studies  are  essential.  Again,  they  can  help  predict  site 
of  lesion,  type  of  injury,  indications  for  temporal  bone 
exploration,  and  prognosis  for  recovery  which  are  all 
essential  for  appropriate  care  of  patients  with  facial 
nerve  paralysis.  ■ 

REFERENCES 

1.  May  M:  The  Facial  Nerve.  New  York,  Thieme  Inc,  1986. 

2.  May  M:  Total  facial  nerve  exploration.  Laryngoscope  1979;89:906. 

3.  Yagi  N:  Comparison  of  thread  test  of  lacrimation  to  Schirmer  test.  Ann 
Otol  Rhinol  Laryngol  1986;122:3. 

4.  May  M,  Harvey  JE:  Salivary  flow;  A prognostic  test  for  facial  paralysis. 
Laryngoscope  1971;81(2):179. 

5.  Alford  BR:  Electrodiagnostic  studies  in  facial  paralysis.  Arch  Otolaryngol 
1967;85:259. 

6.  Dobie  R:  Electrical  and  topognoshc  test  of  the  facial  nerve,  in  Otolaryn- 
gology — Head  and  Neck  Surgery,  Cummigs  C (ed).  St  Louis,  CV  Mosby 
Company,  1986. 

7.  Fisch  U;  Prognostic  value  of  electrical  test  in  acute  facial  paralysis.  Am  } 
Otology  1986;5:494. 


Dr  Duplechain  is  a resident  in  the  Dept  of  Otolaryngology  — Head  and 
Neck  Surgery  at  Tulane  University  Medical  Center  in 

New  Orleans. 

Dr  Blair  is  a professor  of  Otolaryngology  — Head  and  Neck  Surgery  at 
Tulane  University  Medical  Center  in  New  Orleans. 

Reprints  will  not  be  available. 


14  JOURNAL  VOL  140  MAY 


Jackie  Tucker,  LSMSA  President 


AUXILIARY  REPORT 


MEETING  THE  CHALLENGES  OF 
TODAY  FOR  TOMORROW 


JACKIE  C.  TUCKER 


IN  Shel  Silverstein's 
book  of  poems,  A 
Light  in  the  Attic,  there  is 
a poem  entitled  “Ham- 
mock." 

Grandma  sent  the 
hammock 

The  good  Lord  sent 
the  breeze. 

Tm  here  to  do  the 
swinging. 

Now  who's  gonna 
move  the  trees? 

There  are  times  I feel  this  little  verse  could  have  been 
subtitled  "Medicine  Today."  We  need  to  determine 
"who's  gonna  move  the  trees."  It  is  time  that  we 
become  more  responsible  for  meeting  the  challenges 
that  medicine  offers  today. 

A commitment  to  membership  will  be  one  of  the 
major  challenges  our  auxiliary  will  undertake  this  year. 
It  is  imperative  that  we  communicate  the  importance 
of  "belonging"  and  "involvement"  to  every  potential 
auxilian  in  Louisiana.  This  past  year  we  have  formed 


two  new  auxiliaries,  Morehouse  and  Natchitoches, 
with  fantastic  leaders  like  Carol  Chorette,  Melissa 
Smith,  and  Cindy  Barnum.  And  as  recently  as  this 
past  month.  Baton  Rouge  increased  its  membership 
by  116  new  members! 

Success  in  our  legislature  is  another  challenge  to 
which  we  must  make  a major  commitment.  We  need 
more  people  like  Helen  Olivier,  Ann  Reilly  Jones,  and 
Jeanne  Buffet  to  vow  to  work  with  our  legislators  to 
assert  our  positions.  To  implement  this,  we  are  plan- 
ning a statewide  "Day  at  the  Legislature"  where  we 
can  all  convene  together  as  an  impressive  body  to 
contact  our  area  representatives.  We  are  challenged 
to  be  better  communicators.  We  need  to  know  more 
about  each  other,  and  more  about  our  neighboring 
auxiliary  projects.  Patti  Brannan  of  Shreveport  will  be 
working  toward  this  goal  with  a new  format  for  our 
Capsulettes. 

Already  we  have  begun  to  meet  the  challenge  of 
health  and  community  involvement.  Our  members 
have  made  such  positive  impacts  across  our  state  — 
Terry  Anseman  of  Lafayette,  and  Ellouise  Sneed  of 
West  St  Tammany  are  just  two  examples.  These  ladies 
have  led  the  way  in  presenting  outstanding,  vital  ► 


JOURNAL  VOL  140  MAY 


15 


BOOKS  RECEIVED 


health-related  programs  to  our  communities. 

We  must  also  maintain  the  challenge  of  working 
not  only  in  our  local  auxiliaries,  but  in  understanding 
the  importance  of  being  active  in  our  state  and  na- 
tional counterparts.  It  will  be  through  the  united  ef- 
forts of  all  of  us  — whether  we're  from  Rapides,  North 
Central,  Orleans,  Calcasieu  or  St  Landry  — the  com- 
mitments of  auxilians  from  Bossier  to  Hammond,  from 
Terrebonne  to  Ouachita,  and  all  points  in  between. 
It  will  take  the  continuing  interest  and  caring  of  past 
and  present  board  members,  and  the  shared  enthu- 
siasm of  our  spouses  that  will  assure  us  of  meeting 
these  goals. 

Our  relationships  with  each  other,  with  other 
auxiliaries,  and  especially  with  our  Louisiana  State 
Medical  Society,  are  all  key  to  meeting  these  chal- 
lenges fully  prepared.  A team  approach  is  necessary 
in  all  our  plans  — our  support  system  must  be  "built- 
in."  It's  our  chance  to  meet  these  challenges,  and  as 
the  poet  wrote,  "to  move  the  trees." 

Focusing  on  these  challenges  is  a priority  for  me 
this  year.  Working  together  with  people  like  each  of 
you  will  assure  our  success!  ■ 


Mrs  Tucker  (wife  of  Dr  Robert  A.  Tucker)  is  president  of  the  Louisiana 

State  Medical  Society  Auxiliary 


The  JOURNAL  seeks  reviews  of  the  following  books.  Interested 
physicians  should  contact  Frank  J.  Ilardi,  MD,  Book  Review  Editor, 
5000  Highway  190,  Suite  D-3,  Covington,  LA  70433. 

PRACTICAL  MICROSCOPIC  HEMATOLOGY: 

A MANUAL  FOR  THE  CLINICAL  LABORATORY 
AND  CLINICAL  PRACTICE 

Fritz  Heckner,  MD,  H.  Peter  Lehmann,  PhD,  Yuan  S.  Kao, 
MD;  Baltimore,  Urban  & Schwarzenberg  Inc,  1988,  97  pages. 

CLINICAL  ELECTROCARDIOGRAPHY: 

A PRIMARY  CARE  APPROACH 

Ken  Grauer,  MD,  R.  Whitney  Curry,  Jr,  MD;  Oradell,  NJ, 
Medical  Economics  Books,  1987,  544  pages. 

OB/GYN  EMERGENCIES:  THE  FIRST  SIXTY  MINUTES 
Roy  Farrell,  MD  (ed);  Rockville,  MD,  Aspen  Publishers  Inc, 

1986,  340  pages. 

ENDOCERVICAL  CARCINOMA: 

A CERVICOSCOPIC  ATLAS 

Minoru  Ueki,  MD;  St  Louis,  Ishiyaku  Euroamerica  Inc,  1987, 
90  pages. 

THE  CLINICAL  GENETICS  HANDBOOK 

Ruth  Berini  (ed);  Oradell,  N],  Medical  Economics  Books,  1986, 
385  pages. 

INTERPRETING  CARDIAC  DYSRHYTHMIAS 

Marcus  Wharton,  MD,  Nora  Goldschlager,  MD;  Oradell,  NJ, 
Medical  Economics  Books,  1986,  241  pages. 

NEUROLOGY:  PROBLEMS  IN  PRIMARY  CARE 

James  L.  Bernat,  MD,  Frederick  M.  Vincent,  MD;  Oradell, 

NJ,  Medical  Economics  Books,  1987,  656  pages. 

INFORMED  CONSENT:  A SURVIVAL  GUIDE 

Donald  J.  Palmisano,  MD,  JD,  Hebert  J.  Mang  Jr,  JD;  New 

Orleans,  Invictus  Publishing  Co,  1987,  47  pages. 

TO  BE  OR  NOT  TO  BE  HUMAN: 

THE  TRAITS  OF  HUMAN  NATURE 

Ben  Freedman,  MD;  New  York,  Vantage  Press,  1987,  509 

pages. 

THE  AGE  OF  MIRACLES 

Guy  Williams;  Chicago,  Academy  Chicago  Publishers,  1987, 
221  pages. 

PRIMARY  CARE  OF  CANCER 

Edward  A.  Mortimer  Jr,  MD  (ed);  Cleveland,  Case  Western 
Reserve  University  School  of  Medicine,  1987,  190  pages. 

HEALING  INTO  LIFE  AND  DEATH 

Stephen  Levine;  Garden  City,  NY,  Anchor  Press/Doubleday, 

1987,  290  pages. 

SICKLE-CELL  ANEMIA  AND  THALASSEMIA 

Newfoundland,  Canada,  Canadian  Sickle-Cell  Society,  1987. 


16 


JOURNAL  VOL  140  MAY 


CALENDAR 


June 


June  1-4 

9th  Conference  on  Computer  Applications  in  Radiology, 

Hilton  Head  Island,  South  Carolina.  Contact:  Ms.  Janice  Ford, 
Continuing  Education  Coordinator,  Dept  of  Radiology,  Hospital 
of  the  University  of  Pennsylvania,  3400  Spruce  St,  Philadelphia, 
PA  19104;  (215)662-6904,  (215)662-6982. 

June  6 

Annual  Instructional  Course  on  the  Clinical  Application  of 
Hyperbaric  Oxygen,  New  Orleans.  Contact:  Jane  Dunne, 
Undersea  & Hyperbaric  Medical  Society,  9650  Rockville  Pike, 
Bethesda,  MD  20814. 

June  9-12 

17th  Aimual  Scientific  Assembly  of  the  American  College 
of  Emergency  Physicians  State  Chapter  of  California  Inc, 

Rancho  Mirage,  California.  Contact:  CAL/ACEP,  505  N 
Supulveda  Blvd,  #12-14,  Manhattan  Beach,  CA  90266; 
(213)374-4039. 

June  11-12 

Workshop  on  Anesthesia  and  Vital  Organ  Fimction,  Boston. 
Contact:  American  Society  of  Anesthesiologists,  515  Busse  Hwy, 
Park  Ridge,  U 60068. 

June  11-14 

Dermatology  for  Non-Dermatologists,  Myrtle  Beach,  South 
Carolina.  Contact:  Division  of  Dermatology,  Box  3135,  Duke 
University  Medical  Center,  Durham,  NC  27710;  (919)684-2504. 

June  16-18 

33rd  Annual  Great  Smokey  Mountain  Pediatric  Seminar, 

Park  Vista  Hotel,  Gatlinburg,  Tennessee.  Contact:  Dr.  San- 
dra Loucks,  University  of  Tennessee  Medical  Center,  Dept  of 
Pediatrics,  1924  Alcoa  Hwy,  Knoxville,  TX  37920;  (615)544-9331. 

June  16-18 

AIDS  and  Infectious  Disease  Update,  Hilton  Resort,  South 
Padre  Island,  Texas.  Contact:  Scott  and  White  Office  of  Con- 
tinuing Medical  Education,  2401  South  31st  St,  Temple,  TX  76508; 
(817)774-2350. 

June  20-23 

1st  International  Symposium  on  Orbital  Plastic  Surgery,  San 

Francisco.  Contact:  Plastic  Surgery  Educational  Foundation,  233 
N Michigan  Ave,  Suite  1900,  Chicago,  11 60601;  (312)228-9900. 

June  27-29 

Perioperative  Red  Cell  Transfusion,  Bethesda,  Maryland. 


Contact:  National  Institutes  of  Health,  9000  Rockmlle  Pike, 
Bethesda,  MD  20852;  (301)496-2520. 


July 


July  1-5 

2nd  Annual  Family  Practice  Board  Review,  San  Diego.  Con- 
tact: Office  of  Continuing  Medical  Education,  UC  San  Diego  School 
of  Medicine,  M-017,  La  Jolla,  CA  92093;  (619)534-3940. 

July  6-13 

Breast  Imaging  and  Ultrasound,  Alaska  88:  Cruise  the  In- 
land Passage.  Contact:  Medical  Seminars  International  Inc,  21915 
Roscoe  Blvd,  Suite  222,  Canoga  Park,  CA  91304;  (818)719-7380. 

July  14-16 

4th  Annual  Berkshire  Medical  Conference:  Advances  in  Car- 
diology, Hancock,  Massachusetts.  Contact:  Berkshire  AHEC, 
(413)447-2417. 

July  17-22 

Physicians  and  Their  Families:  Balancing  Commitments  to 
Family  and  Profession,  Estes  Park,  Colorado.  Contact:  Jayne 
Roberts,  Conference  Coordinator,  Division  of  Continuing  Educa- 
tion, The  Menninger  Clinic,  Box  829,  Topeka,  KS  66601-0829; 
(800)288-7377. 

July  19-23 

Louisiana  Academy  of  Family  Physicians  Annual  Scientific 
Assembly,  Sandestin  Beach  Hilton,  Destin,  Horida.  Contact: 
LAPP,  4705  Iberville  St,  New  Orleans,  LA  70119. 

July  21  - August  2 

Italy  and  the  Swiss  Alps,  Sponsored  by  INTRAV  and  the 
Louisiana  State  Medical  Society.  Contact:  Anita  Bums,  LSMS, 
1700  Josephine  St,  New  Orleans,  LA  70113;  (504)561-1033, 
(800)462-9508. 

July  24-28 

34th  Armual  Southern  OB-GYN  Seminar,  Asheville,  North 
Carolina.  Contact:  Dr.  George  Schneider,  Ochsner  Clinic,  Dept 
of  OB-GYN,  1514  Jefferson  Hwy,  New  Orleans,  LA  70121; 
(504)838-4031. 

July  24-29 

8th  Annual  Internal  Medicine  Review,  Hilton  Resort,  South 
Padre  Island,  Texas.  Contact:  Scott  & White  (Continuing  Medical 
Education  Office,  2401  South  31st  St,  Temple,  TX  76508; 
(817)774-2350. 


JOURNAL  VOL  140  MAY  19 


IN  OCTOBER  1987,  the  National 
Heart,  Lung  and  Blood  Insti- 
tute (NHLBI),  in  cooperation  with 
the  American  Heart  Association 
and  other  organizations,  launched 
a national  campaign  called  the  Na- 
tional Cholesterol  Education  Pro- 
gram (NCEP).  This  effort  was  in- 
itiated as  a direct  result  of  the 
recommendations  of  the  NHLBI 
Consensus  Conference  on  Lower- 
ing Cholesterol.  The  Consensus 
Conference,  after  careful  considera- 
tion of  all  lines  of  evidence  support- 
ing an  association  between  elevated  serum  cholesterol 
and  coronary  heart  disease  (CHD),  concluded  that 
there  was  a cause-and-effect  relationship  between 
serum  cholesterol  and  CHD  and  that  a decline  in  CHD 
mortality  in  the  United  States  can  be  affected  by  con- 
trol of  hypercholesterolemia.  The  goal  of  the  NCEP  is 
to  help  prevent  Ulness  and  premature  death  from  CHD 
by  reducing  the  number  of  Americans  with  high  serum 
cholesterol.  The  purpose  of  the  NCEP,  in  the  words 
of  James  I.  Cleeman,  MD,  NHLBI  program  coor- 
dinator, "is  to  educate  both  professionals  and  the 
public  to  make  it  clear  how  important  it  is  to  lower  high 
cholesterol  levels  and  to  explain  how  to  go  about  it." 

Each  year,  the  JOURNAL  works  with  the  Physician 
Education  Committee  of  the  Louisiana  Heart  Associa- 
tion to  produce  a special  issue  devoted  to  car- 
diovascular disease.  This  year,  quite  appropriately,  the 
topic  for  this  special  issue  is  the  evaluation  and 
management  of  hypercholesterolemia.  The  Physician 
Education  Committee  of  the  Louisiana  Heart  Associa- 
tion hopes  that  this  issue  will  provide  Louisiana  physi- 
cians with  a strong  impetus  for  implementing  the 
NCEP  recommendations. 

The  background  and  the  scientific  rationale  for 
treatment  of  elevated  serum  cholesterol  are  presented 
by  Drs  Cox  and  Reddy  in  the  first  article.  They  review 
the  evidence  from  genetic,  experimental, 
epidemiological,  and  clinical  studies  linking  cholesterol 
with  CHD.  The  second  article  by  Drs  Leyser  and 
Kucenta  discusses  the  diagnosis  and  evaluation  of 
hypercholesterolemia  including  the  classification  of 


Cholesterol  and 

CORONARY 

HEART 

DISEASE 


20  JOURNAL  VOL  140  MAY 


hyperlipoproteinemias.  This  is  followed  by  an  article 
by  Dr  Lopez  and  Ms  Legardeur  on  the  new  guidelines 
for  the  treatment  of  hyperlipidemia.  These  guidelines, 
based  on  the  recommendations  of  the  NCEP,  provide 
a detailed  set  of  recommendations  to  guide  clinical 
practice.  The  problem  of  dietary  treatment  of  hyper- 
cholesterolemia is 
addressed  by  Ms 
Legardeur  and  Dr 
Lopez  who  give 
practical  approach- 
es to  dietary  ther- 
apy. The  final  arti- 
cle by  Dr  Levine 
focuses  on  drug 
therapy  and  pro- 
vides clear  guide- 
lines on  the  selec- 
tion and  use  of 
pharmacologic 
agents  for  serum 
cholesterol  re- 
duction. 

With  the  launch- 
ing of  the  NCEP, 
preventive  cardio- 
logy has  come  of 
age  and  elevated 
serum  cholesterol 
has  taken  its  right- 
ful place  in  public 
awareness  along- 
side high  blood 
pressure  and  cigar- 
ette smoking.  It  is 
inevitable  that  as 
new  knowledge  ac- 
cumulates, we  will 
make  further  pro- 
gress in  our  fight 
against  CHD.  ■ 


C.  Pratap  Reddy,  MD 

LSU  School  of  Medicine, 
Shreveport 


JOURNAL  VOL  140  MAY  21 


Consider  the 
causative  organisms... 


cefaclor 


250-mg  Pulvules®  t.i.d. 
offers  effectiveness  against 
the  major  causes  of  bacteriai  bronchitis 

Haemophilus  influenzae  and  Streptococcus  pneumoniae 

(ampicillin-susceptible  and  ampicillin-resistant) 


Note:  Ceclor  is  contraindicated  in  patients  with  known  allergy  Penicillin  is  the  usual  drug  of  choice  in  the  treatment  and 
to  the  cephalosporins  and  should  be  given  cautiously  to  prevention  of  streptococcal  infections,  including  the  prophy- 
penicillin-allergic  patients.  laxis  of  rheumatic  fever.  See  prescribing  information. 


Ceclor*  (cefaclor) 

Summary.  Consult  the  package  literature  for 
prescribing  information. 

Indication:  Lower  respiratory  infections, 
inciuding  pneumonia,  caused  by  Streptococcus 
pneumoniae,  Haemophilus  influenzae,  and 
Streptococcus  pyogenes  (group  A /3 -hemolytic 
streptococci). 

Contraindication; 

Known  allergy  to  cephalosporins. 

Warnings: 

CECLOR  SHOULD  BE  AOtifllNISTERED  CAUTIOUSLY  TO 
PENICILLIN-SENSITIVE  PATIENTS.  PENICILLINS  AND  CEPHA- 
LOSPORINS SHOW  PARTIAL  CROSS-ALLERGENICITY.  POSSI- 
BLE REACTIONS  INCLUDEANAPHYLAXIS. 

Administer  cautiously  to  allergic  patients. 
Pseudomembranous  coiitis  has  been 
reported  with  virtually  all  broad-spectrum  anti- 
biotics. It  must  be  considered  in  differential 
diagnosis  of  antibiotic-associated  diarrhea. 
Colon  flora  is  altered  by  broad-spectrum 
antibiotic  treatment,  possibly  resulting  in 
antibiotic-associated  colitis. 


Precautions; 

• Discontinue  Ceclor  in  the  event  of  allergic 
reactions  to  it. 

• Prolonged  use  may  result  in  overgrowth  of 
nonsusceptible  organisms. 

• Positive  direct  Coombs'  tests  have  been  re- 
ported during  treatment  with  cephalosporins. 

• Ceclor  should  be  administered  with  caution  in 
the  presence  of  markedly  impaired  renal  func- 
tion. Although  dosage  adjustments  in  moderate 
to  severe  renal  impairment  are  usually  not 
required,  careful  clinical  observation  and  labo- 
ratory studies  should  be  made. 

• Broad-spectrum  antibiotics  should  be  pre- 
scribed with  caution  in  individuals  with  a his- 
tory of  gastrointestinal  disease,  particularly 
colitis. 

• Safety  and  effectiveness  have  not  been  deter- 
mined in  pregnancy,  lactation,  and  infants  less 
than  one  month  old.  Ceclor  penetrates  mother's 
milk.  Exercise  caution  in  prescribing  for  these 
patients. 

Adverse  Reactions:  (percentage  of  patients) 
Therapy-related  adverse  reactions  are 
uncommon.  Those  reported  include: 


• Gastrointestinal  (mostly  diarrhea):  2.5%. 

• Symptoms  of  pseudomembranous  colitis  may 
appear  either  during  or  after  antibiotic  treat- 
ment. 

• Hypersensitivity  reactions  (including  mor- 
billiform eruptions,  pruritus,  urticaria,  and 
serum-sickness-like  reactions  that  have 
included  erythema  multiforme  [rarely,  Ste- 
vens-Johnson  syndrome]  or  the  above  skin 
manifestations  accompanied  by  arthritis/ 
arthralgia  and,  frequently,  fever):  1 .5%;  usually 
subside  within  a few  days  after  cessation  of 
therapy.  Serum-sickness-like  reactions  have 
been  reported  more  frequently  in  children  than 
in  adults  and  have  usually  occurred  during  or 
following  a second  course  of  therapy  with 
Ceclor.  No  serious  sequelae  have  been 
reported.  Antihistamines  and  corticosteroids 
appear  to  enhance  resolution  of  the  syndrome. 

• Cases  of  anaphylaxis  have  been  reported,  half 
of  which  have  occurred  in  patients  with  a his- 
tory of  penicillin  allergy. 

•As  with  some  penicillins  and  some  other 
cephalosporins,  transient  hepatitis  and  chole- 
static jaundice  have  been  reported  rarely. 

• Rarely,  reversible  hyperactivity,  nerv- 


ousness, insomnia,  confusion,  hypertonia, 
dizziness,  and  somnolence  have  been  reported. 

• Other:  eosinophilia,  2%;  genital  pruritus  or 
vaginitis,  less  than  1%;  and,  rarely,  throm- 
bocytopenia. 

Abnormalities  in  laboratory  results  of  uncertain 
etiology 

• Slight  elevations  in  hepatic  enzymes. 

• Transient  fluctuations  in  leukocyte  count 
(especially  in  infants  and  children). 

• Abnormal  urinalysis;  elevations  in  BUN  or 
serum  creatinine. 

• Positive  direct  Coombs'  test. 

• False-positive  tests  for  urinary  glucose  with 

Benedict's  or  Fehling's  solution  and  ClinitesF 
tablets  but  not  with  Tes-Tape*  (glucose 
enzymatic  test  strip,  Lilly).  [ositbtli 

PA  0709  AMP 

©1987,  ELI  LILLY  AND  COMPANY  CR-5005-B-849318 

Addiliona  I information  agitable  to  the 
profession  on  request  from  EliLitlyand 
Company,  Indianapolis,  Indiana  A6285 

Eli  Lilly  Industries,  Inc 

Carolina,  Puerto  Rico  00630 


CHOLESTEROL  AND  CORONARY 
ATHEROSCLEROSIS 


JAMES  W.  COX  JR,  MD;  C.  PRATAP  REDDY,  MD 


Coronary  heart  disease  (CHD)  is  the  leading  cause 
of  death  in  the  United  States,  accounting  for  more 
than  25%  of  all  deaths.^  A major  primary  risk 
factor  for  CHD  is  elevated  serum  cholesterol  level. 

Although  the  association  between 
hypercholesterolemia  and  CHD  has  been 
recognized  for  many  years,  only  recently  has  it 
been  established  that  a reduction  in  serum 
concentration  of  cholesterol  is  accompanied  by  a 
decreased  risk  for  CHD.  An  abundance  of  genetic, 
experimental,  epidemiologic,  and  clinical  data 
provide  conclusive  evidence  for  a causal 
relationship  between  serum  cholesterol  and 
atherosclerotic  coronary  artery  disease.  It  is  the 
purpose  of  this  article  to  review  the  evidence  for 
cholesterol  and  the  atherosclerosis  connection  and 
briefly  discuss  the  pathogenetic  mechanisms  of 

atherosclerosis. 


Genetic  studies  in  patients  with  familial  hyper- 
cholesterolemia provide  the  most  persuasive 
evidence  for  the  role  of  cholesterol  in  atherosclerosis.^ 
Familial  hypercholesterolemia  occurs  because  of  ab- 
normalities in  gene  encoding  for  low  density  lipopro- 
tein (LDL)  receptors.  In  patients  with  this  inherited 
disorder,  deficiency  of  LDL  receptor  function  leads  to 
accumulation  of  cholesterol  in  the  plasma  and  results 
in  premature  atherosclerotic  coronary  artery  disease. 
Normally,  one  functional  gene  from  each  parent  is 
inherited  for  LDL  receptors.  Patients  with  heterozy- 
gous form  of  famUial  hypercholesterolemia  inherit  one 
normal  gene  and  one  nonfunctioning  gene  for  LDL 
receptors,  and  thus,  possess  only  half  the  normal 
number  of  LDL  receptors.  In  the  homozygous  form 
of  familial  hypercholesterolemia,  there  is  an  absolute 
deficiency  of  LDL  receptors  because  abnormal  genes 
are  inherited  from  both  parents.  One  in  500  persons 
have  heterozygous  form  of  familial  hypercholestero- 
lemia; homozygous  form  is  much  less  commonly  seen. 
Both  forms  of  disease  are  associated  with  very  high 
levels  of  serum  cholesterol  and  premature  athero- 
sclerotic vascular  disease,  but  the  most  fulminant  form 
of  occlusive  vascular  disease  occurs  in  patients  with 


JOURNAL  VOL  140  MAY  23 


the  homozygous  form  of  hypercholesterolemia.  It  is 
thought  that  the  most  commonly  occurring  forms  of 
hypercholesterolemia  probably  represent  a variety  of 
gene  defects  that  become  phenotypically  expressed 
only  in  the  presence  of  certain  environmental  factors. 

EXPERIMENTAL  STUDIES 

In  1913,  on  the  basis  of  his  animal  experiments,  An- 
itschkow proposed  that  hypercholesterolemia  leads 
to  atherosclerosis.^  He  showed  that  a diet  of  pure 
cholesterol  fed  to  rabbits  would  lead  to  hypercholes- 
terolemia and  atherosclerosis  of  the  coronary  arteries 
and  the  aorta.  Subsequent  studies  conducted  in  many 
animal  species  including  non-human  primates  have 
shown  that  hypercholesterolemia  and  atherosclerosis 
can  be  produced  by  feeding  diets  rich  in  saturated 
fats  and  cholesterol  or  containing  bile  acids.  Several 
investigators  have  studied  the  experimental  induction 
of  atherosclerosis  in  cynomolgus  macaques  and  rhe- 
sus monkeys  by  feeding  a cholesterol  rich  diet.^  In 
these  animals,  atherosclerosis  occurs  only  when  high 
levels  of  serum  cholesterol  have  been  achieved,  and 
early  atherosclerotic  lesions  are  seen  in  the  aorta,  and 
the  carotid  and  iliac  arteries.  It  has  been  noted  that 
one  rhesus  monkey  per  300  monkeys  at  risk  per  year 
may  develop  a myocardial  infarction,  a rate  similar  to 
that  seen  in  American  men.  Also  similar  to  man  is 
the  degree  of  coronary  artery  atherosclerosis  at  each 
level  of  plasma  cholesterol  concentration. 

EPIDEMIOLOGIC  STUDIES 

Several  epidemiologic  studies  of  CHD  including  one 
in  Japanese  men  living  outside  Japan^  and  autopsy 
findings  in  young  American  soldiers  killed  in  action 
during  the  Korean  war^  have  strongly  suggested  a 
link  between  diet,  hyperlipidemia,  and  CHD.  How- 
ever, it  was  only  recently  that  convincing  evidence 
for  a direct  association  between  hypercholesterolemia 
and  CHD  was  provided  by  prospective  population 
studies.  The  two  most  notable  studies  in  this  regard 
are  the  Framingham  Study^  and  the  Multiple  Risk 
Factor  Intervention  Trial  (MRFIT)  Study.® 

THE  FRAMINGHAM  STUDY 

The  Framingham  Study^  demonstrated  a direct  cor- 
relation between  cholesterol  levels  and  mortality  from 
cardiovascular  disease.  This  conclusion  was  based  on 

24  JOURNAL  VOL  140  MAY 


the  results  of  a 30  year  follow-up  study  carried  out  in 
1,959  men  and  2,415  women  between  31  and  65  years 
of  age  who  were  free  of  cardiovascular  disease.  In  this 
study,  cardiovascular  death  increased  by  9%  for  each 
10  mg/dl  increase  in  serum  cholesterol. 

THE  MULTIPLE  RISK  FACTOR 
INTERVENTION  TRIAL  STUDY 

The  MRFIT  Study,®  constituting  the  largest  cohort  with 
standardized  serum  cholesterol  measurements  and 
long  term  mortality  follow  up,  showed  a “continuous, 
graded  and  strong"  correlation  between  serum  cho- 
lesterol and  CHD  death  rates.  The  MRFIT  Study  in- 
cluded 356,222  men  between  35  and  57  years  of  age 
who  were  followed  for  six  years.  The  mortality  rate 
due  to  CHD  was  3.5  times  higher  in  patients  with 
serum  cholesterol  levels  greater  than  245  mg/dl  when 
compared  to  patients  with  serum  levels  of  less  than 
181  mg/dl. 

CLINICAL  STUDIES 

Although  the  strong  association  between  cholesterol 
and  coronary  heart  disease  has  been  recognized  for 
many  years,  very  little  was  done  about  it  because 
there  was  no  universally  acceptable  proof  that  low- 
ering the  serum  cholesterol  would  reduce  the  risk  of 
CHD.  A number  of  recent  studies  have  provided  most 
compelling  evidence  that  reducing  blood  cholesterol 
levels  can  lower  the  risk  of  CHD.  These  studies  dem- 
onstrated that  lowering  of  serum  cholesterol  not  only 
decreases  incidence  of  coronary  artery  disease  but  may 
also  slow  or  arrest  the  progression  of  atherosclerotic 
lesions. 

THE  LIPID  RESEARCH  CLINICS 
CORONARY  PRIMARY  PREVENTION 
(LRC-CPP)  TRIAL 

The  LRC-CPP  TriaP  was  a randomized,  placebo  con- 
trolled, double-blind  study  with  two  end  points  being 
heart  attack  and  cardiac  death.  In  this  study,  3,806 
men  with  a serum  cholesterol  level  of  greater  than 
265  mg/dl  and  no  evidence  of  coronary  artery  disease 
were  randomized  into  two  groups.  One  group  was 
treated  with  low  cholesterol  diet  and  cholestyramine 
resin  and  the  other  with  diet  plus  placebo.  All  patients 
were  followed  for  a minimum  of  seven  years.  At  the 
end  of  the  study  period,  the  treatment  group,  com- 


pared  to  the  placebo  group,  showed  an  8%  decrease 
in  total  cholesterol  and  11%  decrease  in  LDL  choles- 
terol; this  lowering  of  cholesterol  resulted  in  24%  re- 
duction in  cardiac  death  and  19%  decrease  in  heart 
attack. 

THE  OSLO  HEART  STUDY 

The  results  of  the  Oslo  Heart  Study^°  were  similar  to 
those  of  the  LRC-CPP  Trial.  In  this  study,  1,232  men 
who  had  no  evidence  of  CHD  were  placed  on  cho- 
lesterol lowering  diet  but  were  not  treated  with  any 
cholesterol  lowering  agents.  During  the  five-year  fol- 
low-up period,  the  serum  cholesterol  level  was  low- 
ered by  approximately  13%  and  the  incidence  rates 
of  fatal  and  nonfatal  myocardial  infarction  and  sud- 
den death  were  reduced  by  47%.  The  investigators 
estimated  that  two-thirds  of  this  beneficial  effect  was 
due  to  lowering  of  cholesterol  and  concluded  that  for 
every  1%  reduction  in  serum  cholesterol  a 2%  reduc- 
tion in  clinical  coronary  events  will  occur. 

THE  NATIONAL  HEART,  LUNG,  AND 
BLOOD  INSTITUTE  (NHLBI)  TYPE  II 
CORONARY  INTERVENTION  STUDY 

The  NHLBI  Type  II  Coronary  Intervention  Study^^ 
was  undertaken  to  test  the  hypothesis  that  lowering 
serum  LDL  cholesterol  reduces  the  rate  of  progression 
of  coronary  artery  disease.  In  this  study,  patients  with 
hypercholesterolemia  and  coronary  artery  disease 
(CAD)  were  randomly  divided  into  two  groups,  one 
treated  with  diet  plus  cholestyramine  and  the  other 
with  placebo  plus  diet.  The  effect  of  treatment  on  the 
progression  of  CAD  was  evaluated  by  angiography 
which  was  performed  in  116  patients  both  before  and 
after  five  years  of  treatment.  Progression  of  CAD  was 
noted  in  49%  of  the  placebo  group  and  in  only  32% 
of  the  cholestyramine  treated  group.  This  difference 
was  statistically  significant. 

PATHOGENESIS  OF  ATHEROSCLEROSIS 

Atherosclerosis  begins  in  early  childhood  and  ather- 
osclerotic plaques  begin  to  appear  at  about  20  years 
of  age.  Lesion  complications  such  as  ulceration, 
thrombosis,  and  hemorrhage  may  develop  after  age 
30. 

The  precise  role  of  cholesterol  in  atherogenesis 
and  the  cellular  mechanisms  involved  in  initiation  of 
atherosclerosis  are  not  completely  understood.  At  least 


three  theories  — lipid  infiltration  hypothesis,  en- 
dothelial injury  hypothesis,  and  monoclonal  hypoth- 
esis — have  been  proposed.  Currently,  a unifying 
hypothesis  known  as  “response  to  injury"  hypothesis 
is  the  most  widely  accepted. This  hypothesis  states 
that  atherosclerosis  is  initiated  in  response  to  injury 
to  arterial  endothelium.  Endothelial  integrity  is  main- 
tained by  both  structural  and  functional  components. 
Previously  it  was  thought  that  a mechanical  injury  to 
the  endothelium  was  necessary  for  initiation  of  ath- 
erosclerotic process.  However,  recent  investigation  has 
shown  that  a denuding  injury  is  not  essential  and  that 
high  levels  of  lipoprotein  may  disrupt  the  functional 
integrity  of  the  endothelium  without  an  apparent  in- 
jury. Experimental  studies  have  revealed  several  pos- 
sible mechanisms  by  which  endothelium  may  be  "in- 
jured" as  a result  of  chronic  exposure  to  elevated  levels 
of  LDL  cholesterol.  Jackson  and  Gotto^^  have  sug- 
gested that  changes  in  the  cholesterol  to  phospholipid 
ratio  of  the  plasma  membranes  of  cells  may  lead  to 
increased  membrane  viscosity.  Such  a change  might 
decrease  the  malleability  of  endothelial  cells  making 
them  more  fragile.  Endothelial  injury  may  also  occur 
as  a result  of  toxic  substances  released  by  oxidized 
LDL  and  by  foam  cells  formed  from  monocytes  and 
macrophages  in  response  to  increased  levels  of  LDL 
cholesterol. Hypercholesterolemia  may  produce  a 
mitogenic  response  in  smooth  muscle  cells  and  in- 
crease monocyte  adhesion  and  chemotaxis  leading  to 
proliferation  of  smooth  muscle  cells  and  development 
of  fatty  streaks. Vasomotor  changes  caused  by  hy- 
percholesterolemia may  also  be  a factor  in  the  path- 
ogenesis of  atherosclerosis.  In  rabbits  fed  a high  cho- 
lesterol diet,  acetylcholine  induced  endothelium- 
dependent  relaxation  can  be  diminished  or  converted 
to  contraction.^^  Several  other  factors  including  plate- 
let and  endothelial  cell  derived  growth  factors  and 
prostaglandins  also  appear  to  play  an  important  role 
in  the  pathogenesis  of  atherosclerosis.^^  A discussion 
of  these  factors  and  their  regulating  mechanisms  is 
beyond  the  scope  of  this  article. 

SUMMARY 

The  association  of  hypercholesterolemia  and  coronary 
heart  disease  is  well  established.  The  mechanisms  by 
which  hypercholesterolemia  initiates  and  propagates 
atherosclerosis  are  not  fully  understood  but  are  under 
active  investigation.  There  is  now  incontrovertible 
proof  that  reducing  serum  cholesterol  levels  will  re- 

JOURNAL  VOL  140  MAY  25 


suit  in  reduced  mortality  and  morbidity  from  coronary 
heart  disease.  Beneficial  effects  can  be  obtained  by 
both  primary  prevention  in  patients  with  no  history 
of  cardiovascular  disease  and  secondary  prevention 
in  patients  with  known  coronary  artery  disease.  ■ 

REFERENCES 

1.  Inter-Society  Commission  for  Heart  Disease  Resources;  Optimal  re- 
sources for  primary  prevention  of  atherosclerotic  disease.  Circulation 
1984;70:153A. 

2.  Goldstein  JL,  Brown  MS:  Regulation  of  low  density  lipoprotein  receptors: 
Implications  for  pathogenesis  and  therapy  of  hypercholesterolemia  and 
atherosclerosis.  Circulation  1987;76(3):504-507. 

3.  Anitschkow  NN:  A history  of  experimentation  on  arterial  atherosclerosis 
in  animals,  in  Cowdry's  Arterios,  ed  2,  Blumenthal  HT  (ed).  Springfield, 
ni,  Charles  C Thomas,  1967,  p 21. 

4.  Jokinen  MP,  Clarkson  TB,  Prichard  RW:  Animal  models  of  atheroscle- 
rosis research.  Exp  Mol  Pathol  1985;42:1. 

5.  Robertson  TL,  Kato  H,  Gordon  T,  et  al:  Epidemiologic  studies  of  coronary 
heart  disease  and  stroke  in  Japanese  men  living  in  Japan  and  Hawaii. 
Am  } Cardiol  1977;39:244-249. 

6.  Enos  WE,  Holmes  RH,  Beyer  J:  Coronary  disease  among  United  States 
soldiers  killed  in  action  in  Korea.  JAMA  1953;152:1090-1093. 

7.  Anderson  KM,  CasteUi  WP,  Levy  D:  Cholesterol  and  mortality:  30  years 
follow-up  from  the  Framingham  Study.  JAMA  1987;254:2176-2180. 

8.  Stamler  J,  Wentworth  D,  Neaton  JD:  Is  relationship  between  serum  cho- 
lesterol and  risk  of  premature  death  from  coronary  heart  disease  con- 
tinuous and  graded?  Findings  in  356,222  primary  screenees  of  the  Mul- 
tiple Risk  Factor  Interventional  Trial  (MRFIT).  JAMA  1986;256:2823. 

9.  Lipid  Research  Clinics  Program,  The  Lipid  Research  Clinics  Coronary 
Primary  Prevention  Trial  Results  II.  The  relationship  of  reduction  in 
incidence  of  coronary  heart  disease  to  cholesterol  lowering.  JAMA 
1984;251:365-374. 

10.  Hjermann  I,  Velve  Byre  K,  Holme  I,  et  al:  Effect  of  diet  and  smoking  on 
the  incidence  of  coronary  heart  disease:  Report  from  Oslo  Study  Group 
of  a randomized  trial  in  healthy  men.  Lancet  1981;2:1303-1310. 

11.  Levy  RI,  Brensike  JF,  Epstein  SE,  et  al:  The  influence  of  changes  in  lipid 
values  induced  by  cholestyramine  and  diet  on  progression  of  coronary 
artery  disease:  Results  of  the  NHLBI  Type  II  coronary  intervention  study. 
Circulation  1984;69:325. 

12.  Ross  R;  The  pathogenesis  of  atherosclerosis  — an  update.  N Engl  J Med 
1986;314:488. 

13.  Jackson  RL,  Gotto  AM  Jr:  Hypothesis  concerning  membrane  structure, 
cholesterol,  and  atherosclerosis,  in  Atherosclerosis  Reviews,  Padetti  R,  Gotto 
AM  Jr  (eds).  New  York,  Raven  Press,  1976,  vol  1,  pp  1-21. 

14.  Cathcart  MK,  Morel  DW,  Chisolm  GM  III:  Monocytes  and  neutrophils 
oxidize  low  density  lipoprotein  making  it  cytotoxic.  J Leukocyte  Biol 
1984;38:341-350. 

15.  Ibeugwe  JK,  Susuki  H:  Protective  action  of  elastase  on  changes  in  me- 
chanical properties  of  vascular  smooth  muscles  during  atherosclero- 
genesis  in  hypercholesterolemic  rabbits.  Arch  Int  Pharmacodyn  Ther 
1987;287:48-64. 

16.  Clarkson  TB,  Weingand  KW,  Kaplan  OR,  et  al;  Mechanisms  of  athero- 
genesis.  Circulation  1987;76  (suppl  1),  1-20. 


Dr  Cox,  a fellow  in  cardiology,  is  affiliated  with  the  Dept  of  Medicine, 
Cardiology  Section,  at  LSU  School  of  Medicine  in  Shreveport. 

Dr  Reddy,  a professor  of  medicine,  is  the  associate  chief  of  cardiology  at 

LSU  School  of  Medicine  in  Shreveport. 

Reprint  requests  should  be  sent  to  C.  Pratap  Reddy,  MD,  Professor  of 
Medicine,  Cardiology  Section,  LSU  School  of  Medicine,  PO  Box  33932, 

Shreveport,  LA  70113. 


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26  JOURNAL  VOL  140  MAY 


DIAGNOSIS  AND  EVALUATION  OF 
HYPERCHOLESTEROLEMIA 


LARRY  J.  LEYSER,  MD;  BRYAN  LUCENTA,  MB 


The  primary  lipids  in  plasma  are  cholesterol  and 
triglycerides.  Cholesterol  is  an  essential  component 
in  cellular  metabolism,  and  triglycerides  are  an 
important  source  of  energy.  Although  vital  to  the 
functioning  of  many  of  the  body's  tissues,  the 
lipids  are  insoluble  in  water  and  must  be 
transported  to  cells  by  other  molecules.  These 
transporting  molecules,  complex  macromolecular 
aggregations  of  lipid  and  protein,  are  known  as 
lipoproteins.  Abnormalities  in  the  synthesis  and 
degradation  of  plasma  lipoproteins  are  related  to 
disorders  of  lipoprotein  metabolism.  The  hallmark 
of  lipoprotein  disorders  is  hyperlipidemia  or  the 
elevation  of  plasma  cholesterol  and/or  triglyceride 
concentrations.  These  abnormalities  may  result 
from  primary  inborn  errors  of  metabolism  or  may 
be  secondary  to  a variety  of  other  disease  states.^ 
The  purpose  of  this  article  is  to  review  the 
classification,  diagnosis,  and  evaluation  of 
lipoprotein  disorders. 


The  four  major  lipoprotein  classes  are  defined  ac- 
cording to  their  density  on  ultracentrifugation. ^ 

1.  Chylomicrons.  These  transport  dietary  fat  (as 
triglycerides)  and  a small  amount  of  cholesterol  from 
the  intestine  to  the  plasma.  The  triglycerides  are  re- 
moved by  lipoprotein  lipase  and  stored  in  fat  cells  as 
fatty  acids.  A remnant  remains  which,  unless  re- 
moved by  the  Uver,  is  thought  by  some  investigators 
to  have  an  atherogenic  capability  similar  to  thaf  of 
low-density  lipoproteins. 

2.  Very  low  density  lipoproteins  (VLDL).  These  are 
secreted  by  the  liver  and  they  transport  triglycerides 
and  a small  amount  of  cholesterol.  Lipoprotein  lipase 
removes  triglycerides  from  VLDL  which  are  then  me- 
tabolized in  the  liver  with  low-density  lipoprotein  as 
the  end  product. 

3.  Low-density  lipoproteins  (LDL).  These  are  the 
end  product  of  VLDL  metabolism,  and  some  LDL  is 
secreted  directly  into  the  plasma.  Low-density  lipo- 
proteins are  the  major  carriers  of  cholesterol  and  are 
closely  linked  to  atherogenesis.  The  amount  of  LDL 
taken  up  by  the  cells  is  controlled  by  LDL  "receptors" 
located  on  the  ceU  membrane  and  deficiency  of  these 
receptors  results  in  elevated  levels  of  plasma  LDL 
cholesterol. 


JOURNAL  VOL  140  MAY  27 


TABLE  1 

CLASSIFICATION  AND  CHARACTERISTICS  OF  HYPERLIPOPROTEINEMIAS 

Major  Elevation  in  Plasma 

Phenotype 

Genotype 

Lipoprotein 

Lipid 

1 

Familial  Hyperchylomicronemia 

Chylomicrons 

Triglyceride 

lla 

Familial  Hypercholesterolemia  (homozygous  or  heterozygous) 

LDL* 

Cholesterol 

Familial  Combined  Hyperlipidemia 

LDL 

Cholesterol 

Polygenic  Hypercholesterolemia 

LDL 

Cholesterol 

Mb 

Familial  Hypercholesterolemia 

LDL 

Cholesterol 

Familial  Combined  Hyperlipidemia 

VLDLt 

Triglyceride 

III 

Familial  Dysbetalipoproteinemia 

IDLt 

Cholesterol 

Triglyceride 

IV 

Familial  Hypertriglyceridemia 

VLDL 

Triglyceride 

Familial  Combined  Hyperlipidemia 

LDL 

Cholesterol 

V 

Familial  Type  V 

Chylomicrons 

Triglyceride 

Familial  Hypertriglyceridemia 

VLDL 

Cholesterol 

* Low  density  lipoprotein 
t Very  low  density  lipoprotein 
t Intermediate  density  lipoprotein 

4.  High-density  lipoproteins  (HDL).  These  are  the 
second  major  carrier  of  cholesterol  and  are  thought 
to  be  responsible  for  the  transport  of  cholesterol  to 
the  liver  for  secretion  in  the  bile.  High  levels  of  HDL 
are  thought  to  be  protective  against  atherosclerosis. 

DEFINITION  OF  HYPERLIPIDEMIA 

Traditionally,  hyperlipidemia  has  been  diagnosed 
when  a person's  serum  cholesterol  or  triglyceride  lev- 
els exceeded  the  95th  percentile  for  his  (her)  age  and 
sex.  This  definition  has  been  revised  and  new  guide- 
lines for  the  diagnosis  of  hypercholesterolemia  have 
been  provided  by  the  National  Institutes  of  Health 
Cholesterol  Consensus  Development  Conference.^ 

RISK  FOR  CORONARY  HEART 
DISEASE 

Atherosclerosis  and  coronary  heart  disease  are  strongly 
associated  with  increased  plasma  cholesterol  levels, 
and  the  degree  of  risk  for  coronary  heart  disease  is 


directly  related  to  the  patient's  plasma  lipid  levels. 
For  determining  such  risk  one  must  adhere  to  the 
National  Cholesterol  Education  Program  recommen- 
dations.^ According  to  these  recommendations,  a 
serum  cholesterol  level  of  less  than  200  mg/dl  carries 
no  risk  for  coronary  heart  disease,  a level  between 
200  mg/dl  and  230  mg/dl  carries  minimal  risk,  and  a 
level  of  equal  to  or  greater  than  240  mg/dl  carries  high 
risk.  Hypertriglyceridemia  is  present  when  triglyc- 
eride levels  exceed  250  mg/dl;  triglyceride  concentra- 
tions of  greater  than  500  mg/dl  are  considered  high 
while  levels  between  250  mg/dl  and  500  mg/dl  are 
considered  borderline  high. 

CLASSIFICATION  OF 
HYPERLIPOPROTEINEMIAS 

In  many  patients,  hyperlipoproteinemia  is  the  result 
of  overconsumption  of  dietary  fat,  but  in  others  this 
may  be  genetically  determined.  Some  of  these  dis- 
orders arise  from  inherited  defects.  The  most  common 
of  these  are  polygenic  hypercholesterolemia,  endog- 


28  JOURNAL  VOL  140  MAY 


enous  hypertriglyceridemia,  familial  hypercholester- 
olemia, and  familial  combined  hyperlipidemia.  A less 
common  type  is  mixed  hyperlipidemia. 

HyperUpoproteinemias  are  classified  on  the  basis 
of  the  specific  lipoprotein  represented  in  the  increased 
plasma  lipid  values.  This  classification  (Table  1)  de- 
vised by  Fredrickson  et  al^  is  based  on  laboratory 
measurements  of  lipoproteins  but  is  useful  in  making 
certain  clinical  correlations. 

SECONDARY  HYPERLIPIDEMIA 

In  some  patients,  hyperlipidemia  may  be  secondary 
to  another  disease,  a metabolic  disorder,  or  to  the  use 
of  certain  drugs.  These  causative  factors  are  listed  in 
Table  2.  The  hypercholesterolemia  due  to  these  etiol- 
ogies can  usually  be  modified  by  treatment  of  the 
disease  process,  correction  of  the  metabolic  abnor- 
mality, or  discontinuation  of  the  drug  eliciting  the 
abnormality. 

CLINICAL  MANIFESTATIONS 

Hypercholesterolemia  presenting  as  increased  LDL 
cholesterol  and  normal  triglyceride  levels  can  be  found 
in  familial  hypercholesterolemia,  familial  combined 
hyperlipidemia,  and  polygenic  hypercholesterolemia. 
Elevated  cholesterol  also  occurs  with  broad  beta  dis- 
ease (type  III  hyperlipoproteinemia)  and  lipoprotein 
lipase  deficiency. 

Familial  hypercholesterolemia  is  transmitted  as 
an  autosomal  dominant  trait  with  both  homozygous 
and  heterozygous  forms  and  is  characterized  by  in- 
creased LDL  cholesterol  and  normal  or  mildly  ele- 
vated plasma  triglyceride  levels.  The  patient  with  the 
homozygous  form  of  disease  presents  early  in  child- 
hood with  planar,  tuberous,  and  tendon  xanthomas.^ 
Planar  xanthomas  are  recognized  as  yellow  lesions  in 
the  finger  web  spaces  and  behind  the  knees.  The  het- 
erozygous form  of  this  disorder  has  lower  levels  of 
plasma  cholesterol  (280  mg/dl  to  550  mg/dl)  and  may 
not  present  with  tendon  xanthomas  until  later  in  life. 
The  xanthomas  are  due  to  insidious  deposition  of  LDL 
cholesterol  in  the  skin  and  tendons.  These  patients 
have  accelerated  atherosclerotic  cardiovascular  dis- 
ease and  may  present  with  valvular  and  supravalvular 
stenosis,  and  early  myocardial  infarction.  Diagnosis 
of  familial  forms  can  be  made  by  skin  biopsies  and 
skin  fibroblast  studies. 

Familial  combined  hyperlipidemia  is  an  autoso- 


TABLE 2 

CAUSES  OF  SECONDARY  HYPERLIPOPROTEINEMIA 


Hypothyroidism 
Diabetes  mellitus 
Nephrotic  syndrome 
Obstructive  liver  disease 
Glycogen  storage  disease 
Myelomas 

Cushing’s  syndrome 
Hyperuricemia 


mal  dominant  inherited  disorder  characterized  by  an 
overproduction  of  VLDL  and  LDL  by  the  Ever.  One 
may  see  a type  Ila  phenotype  (increased  LDL  choles- 
terol), type  Ilb  phenotype  (increased  VLDL  and  LDL 
cholesterol)  or  a type  IV  phenotype  (singular  eleva- 
tion of  VLDL  cholesterol).  Tendon  xanthomas  are  in- 
variably absent  in  this  disorder  but  eruptive  xantho- 
mas may  occur  in  those  with  hypertriglyceridemia 
and  diabetes  mellitus.  The  laboratory  diagnosis  is  made 
by  demonstration  of  different  lipoprotein  phenotypes 
in  different  family  members. 

Combined  hypercholesterolemia  and  hypertri- 
glyceridemia occurs  in  type  lib  phenotypes  with  el- 
evated LDL  and  VLDL,  or  may  indicate  the  presence 
of  abnormal  chylomicron  and  VLDL  remnants  that 
are  typical  of  dysbetalipoproteinemia  (type  III  hyper- 
lipoproteinemia). To  differentiate  between  type  lib 
and  type  III,  one  must  use  ultracentrifugal  separation 
of  the  VLDL  component.  Clinically,  these  patients 
have  palmar  and  tuberous  xanthomas,  and  tubero- 
eruptive  xanthomas  on  the  buttocks.  There  is  an  in- 
creased incidence  of  coronary  and  peripheral  vascular 
disease  thought  to  be  caused  by  the  uptake  of  VLDL 
and  LDL  cholesterol  by  the  arterial  smooth  muscle 
cells  and  macrophages.  This  disorder  is  usually  as- 
sociated with  obesity,  diabetes  meUitus,  hypothy- 
roidism, or  a coexistent  familial  hyperlipidemia. 

EVALUATION 

For  the  determination  of  serum  lipid  levels,  blood 
samples  should  be  obtained  from  the  patient  after  a 
12-hour  fast.  Total  serum  cholesterol,  triglycerides, 
and  HDL  levels  should  be  measured  during  the  initial 
screening.  If  the  values  are  normal  at  initial  screening. 


JOURNAL  VOL  140  MAY  33 


they  should  be  repeated  every  five  years.  If  an  ab- 
normality is  found  at  initial  evaluation,  this  should 
be  confirmed  by  a second  test  followed  by  identifi- 
cation of  the  underlying  lipoprotein  abnormality.  The 
level  of  LDL  cholesterol  can  be  deduced  by  using  the 
following  formula  developed  by  the  Lipid  Research 
Clinics  Program:  LDL  cholesterol  = total  cholesterol 
— HDL  cholesterol  — triglyceride  level/5.  ■ 

REFERENCES 

1.  Havel  RJ,  et  al:  Lipoprotein  and  lipid  transport,  in  Metabolic  Control  and 
Disease,  ed  8,  Bondy  PK,  Rosenberg  LE  (eds).  Philadelphia,  W.B.  Saun- 
ders, 1980,  chap  7,  pp  393-494. 

2.  Peters  WL,  Goroll  AH:  The  evaluation  and  treatment  of  hypercholester- 
olemia in  primary  care  practice.  / Gen  Intern  Med  1986;1(3):183-195. 

3.  Consensus  Conference  [National  Institutes  of  Health  Cholesterol  Con- 
sensus Development  Conference]:  Lowering  blood  cholesterol  to  prevent 
heart  disease.  JAMA  1985;253:280. 


4.  Lipid  Research  Clinics  Program:  The  Lipid  Research  Clinics  — Coronary 
Primary  Prevention  Trial  (CPPT)  Results.  I.  Reduction  in  incidence  of 
coronary  heart  disease  to  cholesterol  lowering.  II.  The  relationships  or 
reductions  in  incidence  of  coronary  heart  disease  to  cholesterol  lowering. 
JAMA  1984;251:351. 

5.  Fredrickson  DS,  Levy  RI,  Lees  RS:  Fat  transport  in  lipoproteins  — an 
integrated  approach  to  mechanism  and  disorders.  N Engl  J Med  1967;276:34- 
281. 

6.  Weidman  W,  Kwiterovich  Jr  P:  Diagnosis  and  treatment  of  primary  hy- 
perlipidemia in  childhood.  Circulation  1986;74:1181A-1188A. 


Dr  Leyser  is  assistant  professor  of  medicine  in  the  Dept  of  Medicine, 
Cardiology  Section,  at  LSU  School  of  Medicine  in  New  Orleans. 

Dr  Lucenta,  a fellow  of  cardiology,  is  also  affiliated  with  the  Dept  of 
Medicine,  Cardiology  Section,  at  LSU  School  of  Medicine  in 

New  Orleans. 

Reprint  requests  should  be  sent  to  Jjirry  J.  Leyser,  MD,  LSU  School  of 
Medicine,  Dept  of  Medicine,  Section  of  Cardiology,  1542  Tulane  Ave, 

New  Orleans,  LA  70112. 


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34  JOURNAL  VOL  140  MAY 


NEW  GUIDELINES 
FOR  THE  TREATMENT  OF 
HYPERLIPIDEMIA  IN  ADULTS 


ALFREDO  LOPEZ-S,  MD,  PhD;  BARBARA  Y.  LEQARDEUR,  MPH 


High  blood  cholesterol  values  have  been  shown  to 
be  a major  risk  factor  for  coronary  heart  disease.  In 
an  attempt  to  diminish  this  risk,  newly  developed 
guidelines  have  been  proposed  by  the  National 
Heart  and  Lung  Institute  in  cooperation  with  the 
American  Heart  Association  and  other  health 
organizations.  To  educate  physicians  in  the 
detection,  evaluation,  and  treatment  of  individuals 
with  elevated  blood  cholesterol  levels,  it  is 
recommended  that  all  adults  over  20  years  of  age 
be  tested  for  their  serum  cholesterol  levels  as  part 
of  a regular  evaluation  of  risk  factors.  Step-wise 
recommendations  are  given  for  the  evaluation  and 
treatment  of  those  individuals  found  to  be  at  risk 
because  of  their  serum  cholesterol  values. 


CORONARY  HEART  DISEASE  (CHD)  continues  to  be 
the  major  cause  of  death  in  the  United  States, 
and  Louisiana  is  a state  with  one  of  the  highest  death 
rates  for  the  disease.^  Hypercholesterolemia  is  one  of 
the  major  risk  factors  of  this  disease  and  there  is  evi- 
dence of  high  incidence  of  hyperlipidemia  in  the  Lou- 
isiana population. 2 The  participants  of  the  Consensus 
Conference  on  Lowering  Blood  Cholesterol  to  Prevent 
Coronary  Heart  Disease,  sponsored  by  the  National 
Institutes  of  Health  (NIH),  agreed  that  the  cause-and- 
effect  relationship  between  blood  cholesterol  and  CHD 
is  related,  that  a decline  in  CHD  mortality  in  the  United 
States  can  be  effected  by  control  of  hypercholestero- 
lemia, and  that  the  National  Heart,  Lung  and  Blood 
Institute  (NHLBI)  should  mount  a national  cholesterol 
education  program  for  both  physicians  and  the  pub- 
lic.^ As  a result  of  their  recommendations,  the  NIH 
and  the  American  Heart  Association  (AHA),  along 
with  multiple  other  cooperating  governmental, 
professional,  and  voluntary  health  organizations  have 
launched  an  ambitious  project  — the  National  Cho- 
lesterol Education  Program.  It  is  aimed  at  educating 
physicians  and  the  general  public  regarding  hyper- 
cholesterolemia. For  this  purpose,  simple  guidelines  ^ 


JOURNAL  VOL  140  MAY  35 


Fig.  Guidelines  for  the  treatment  of  hyperlipidemia 
in  adults. 


r 


i 


i 


r 


1 


have  been  developed  for  screening,  diagnosis,  and 
treatment  of  individuals  at  different  levels  of  risk  based 
on  their  cholesterol  values  and  the  presence  or  ab- 
sence of  other  risk  factors  for  CHD  (Fig).  These  guide- 
lines are  compatible  with  recently  developed  methods 
that  allow  fast  (three  to  eight  minutes)  measurement 
of  cholesterol  levels  in  small  amounts  of  blood  (10-20 
fxl  obtained  by  finger  stick)  and  new  information  re- 


garding the  benefits  of  diet  and  drug  therapy  in  the 
treatment  of  hyperlipidemia. 

DETECTION  AND  CLASSIFICATION  OF 
SERUM  CHOLESTEROL 

The  AHA  endorsed  the  recommendation  that  aU  adults 
over  age  20  should  be  tested  for  their  serum  choles- 
terol, which  can  be  obtained  in  a fasting  or  non-fasting 
state. 

Individuals  with  total  serum  cholesterol  less  than 
200  mg/dl  are  considered  to  have  "desirable  blood 
cholesterol,"  and  are  encouraged  to  follow  the  AHA 
diet  and  lead  a healthy  lifestyle.  They  should  have 
their  serum  cholesterol  repeated  in  five  years. 

When  the  serum  cholesterol  level  is  200  mg/dl,  it 
needs  to  be  confirmed  by  a new  determination  in  one 
to  eight  weeks.  If  this  confirmation  value  is  within  30 
mg/dl  of  the  first  one,  the  average  of  the  two  tests  is 
used  for  decisions  following  the  guidelines.  If  the  sec- 
ond value  differs  from  the  first  by  more  than  30  mg/ 
dl,  a third  determination  should  be  made  in  another 
one  to  eight  weeks  and  the  three  values  averaged.  If 
this  averaged  value  of  cholesteroTis  between  200  mg/ 
dl  and  239  mg/dl,  the  value  is  called  "borderline  high 
total  cholesterol,"  and  if  it  is  above  240  mg/dl,  the 
value  is  called  “high  total  cholesterol."  In  those  in- 
dividuals with  borderline  high  (200  mg/dl  to  239  mg/ 
dl)  value  of  cholesterol,  their  risk  factor  status  should 
be  evaluated.  A "high  risk"  status  is  defined  accord- 
ing to  the  AHA  guidelines  as  the  presence  of  definite 
CHD  or  two  other  risk  factors.  The  risk  factors  for 
CHD  include:  1)  male  sex,  2)  family  history  of  pre- 
mature CHD,  3)  cigarette  smoking,  4)  hypertension, 
5)  low  HDL-cholesterol  (<35  mg/dl),  6)  diabetes  mel- 
litus,  and  7)  severe  obesity  (>30%  overweight). 

Those  other  individuals  with  "borderline  high" 
serum  cholesterol  (200  mg/dl  to  239  mg/dl)  but  with- 
out CHD  or  two  risk  factors,  do  not  require  special 
treatment,  and  are  advised  to  follow  the  AHA  diet 
along  with  a healthy  lifestyle.  Educational  material 
should  be  given  to  them,  and  their  serum  cholesterol 
should  be  repeated  in  one  year. 

If  the  patient  has  borderline  high  cholesterol  and 
is  at  high  risk  (presence  of  CHD  or  two  risk  factors), 
lipoprotein  analysis  needs  to  be  performed. 

In  patients  with  "high  total  serum  cholesterol" 
(over  240  mg/dl),  lipoprotein  analysis  needs  to  be  per- 
formed. The  ultimate  classification  of  a patient's  cho- 


36  JOURNAL  VOL  140  MAY 


lesterol  status  will  be  based  on  the  low  density  lipo- 
protein (LDL)-cholesterol  level. 

DETERMINATION  AND 
CLASSIFICATION  OF  LDL 
CHOLESTEROL 

Determination.  To  determine  LDL  cholesterol  it  is  nec- 
essary to  order  a 12-hour  fasting  lipid  analysis  con- 
sisting of  total  cholesterol,  high  density  lipoprotein 
(HDL)-cholesterol,  and  triglycerides.  From  the  results 
of  this  test,  LDL-cholesterol  can  be  calculated  as  fol- 
lows: 

LDL-cholesterol  = Total  cholesterol  — 
(HDL-cholesterol  + triglycerides/5) 

It  is  advisable  to  perform  two  or  three  determi- 
nations, one  to  eight  weeks  apart  and  establish  an 
average  LDL-cholesterol  level. 

Classification.  A desirable  LDL-cholesterol  is  be- 
low 130  mg/dl.  Individuals  with  “desirable"  LDL-cho- 
lesterol levels  are  advised  to  repeat  total  cholesterol 
level  in  five  years  and  to  follow  the  AHA  diet  and  to 
lead  a healthy  lifestyle. 

Borderline  high-risk  LDL-cholesterol  is  an  LDL- 
cholesterol  level  of  130  mg/dl  to  159  mg/dl.  For  indi- 
viduals with  borderline  high  risk  LDL-cholesterol  lev- 
els and  evidence  of  CHD  or  two  risk  factors,  it  is 
recommended  that  they  follow  the  Step  I diet  and 
have  their  cholesterol  reevaluated  annually. 

Those  individuals  with  borderline  LDL-choles- 
terol values  and  presence  of  CHD  or  two  risk  factors 
should  be  treated  the  same  as  individuals  with  high 
risk  LDL-cholesterol. 

High  risk  LDL-cholesterol  is  a level  of  over  160  mg/ 
dl.  These  individuals  require  a complete  clinical  eval- 
uation to  determine  secondary  or  genetic  causes  for 
their  hyperlipidemia  and  should  enter  a cholesterol- 
lowering therapy  (diet  alone  or  diet  plus  drugs)  in 
order  to  achieve  an  LDL-cholesterol  level  of  less  than 
160  mg/dl  when  no  CHD  risk  factors  are  present  and 
a level  of  less  than  130  mg/dl  in  the  presence  of  def- 
inite CHD  or  two  other  risk  factors. 

SUMMARY 

According  to  the  new  guidelines  of  the  NHLBI  and 
AHA,  cholesterol  determinations  should  be  done  in 
all  adults  over  20  years  of  age.  On  the  basis  of  cho- 


lesterol level  and  the  presence  or  absence  of  CHD  or 
two  other  risk  factors,  individuals  will  be  classified  as 
having  desirable,  borderline-high,  or  high-risk  cho- 
lesterol levels.  A decision  to  start  a patient  on  active 
medical  therapy  for  high  cholesterol  levels  should  be 
made  on  the  basis  of  the  LDL-cholesterol  classifica- 
tion, not  the  serum  total  cholesterol.  ■ 

REFERENCES 

1.  Oalman  MC:  Coronary  Heart  Disease  in  Louisiana.  / La  State  Med  Soc 
1974;126:39. 

2.  Lopez-S  A:  Coronary  Heart  Disease  Detection  Program.  / La  State  Med  Soc 
1974;126:43. 

3.  NIH  Consensus  Development  Conference  Summary.  JAMA 
1985;253(14);2080. 


Dr.  Lopez-S  is  a professor  of  medicine  in  the  Dept  of  Medicine, 
Nutrition  Section,  at  LSU  School  of  Medicine  in  New  Orleans. 

Ms  Legardeur  is  a registered  dietitian  and  an  assistant  professor  of 
clinical  medicine  in  the  Dept  of  Medicine,  Nutrition  Section,  at 
LSU  School  of  Medicine  in  New  Orleans. 

Reprints  will  not  be  available. 


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JOURNAL  VOL  140  MAY  37 


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38  JOURNAL  VOL  140  MAY 


DIETARY  TREATMENT  OF 
ELEVATED  SERUM  CHOLESTEROL 


BARBARA  Y.  LEGARDEUR,  MPH;  ALFREDO  LOPEZ-S,  MD,  PhD 


Diet  is  essential  to  the  management  of  high  blood 
cholesterol  in  patients.  Dietary  factors  which 
contribute  to  increased  serum  cholesterol  levels 
include  a high  intake  of  saturated  fatty  acids,  a 
relatively  high  intake  of  cholesterol,  and  obesity. 
A two-step  diet  approach  has  been  developed  by 
members  of  the  National  Cholesterol  Education 
Program  and  the  American  Heart  Association.  This 
two-step  approach  progressively  reduces  the  intake 
of  saturated  fatty  acids  and  dietary  cholesterol,  as 
well  as  controlling  the  level  of  calories,  if 
warranted.  Physicians  are  advised  to  become 
knowledgeable  of  the  Step  1 Diet  and  to 
implement  it  in  appropriate  patients.  The  major 
components  of  the  Step  1 Diet  include  limitation 
of  meat,  fish,  and  poultry,  up  to  6 oz  daily;  use  of 
low-fat  dairy  products,  no  more  than  three  egg 
yolks  per  week;  and  up  to  6 to  8 teaspoons  of  fats 
and  oils  daily.  The  guidelines  also  recommend 
increased  use  of  fruits,  vegetables,  and  grain 

products  in  the  diet. 


Diet  is  the  cornerstone  of  management  for  the  per- 
son with  high  or  borderline  high  blood  choles- 
terol. For  many  people,  this  will  necessitate  perma- 
nent changes  in  eating  behavior  rather  than  temporary 
modification  of  food  intake.  The  factors  in  the  Amer- 
ican diet  that  contribute  to  increased  serum  choles- 
terol levels  are  a high  intake  of  saturated  fatty  acids, 
relatively  high  intake  of  dietary  cholesterol,  and  ex- 
cess calories  that  exceed  the  body's  requirement  re- 
sulting in  obesity.^ 

DIETARY  FAT 

In  the  average  American  diet,  approximately  13%  to 
15%  of  total  calories  come  from  saturated  fatty  acids. 

It  is  estimated  that  the  proportion  of  saturated  fatty 
acids  in  the  average  Louisianan  diet  is  similar  to  that 
of  the  average  American  diet.^'^  In  general,  animal 
fats  (butter,  beef  and  pork  fat)  contribute  most  of  the 
saturated  fatty  acids  to  diet  but  a significant  portion 
may  come  from  certain  vegetable  oils  (palm,  palm 
kernel,  and  coconut  oil). 

The  polyunsaturated  fatty  acids,  especially  lino- 
leic  acid,  have  been  shown  to  lower  serum  cholesterol 
when  substituted  for  saturated  fatty  acids.  However,  ^ 


JOURNAL  VOL  140  MAY  39 


Cholesterol 

(mg/IOOgm 

food)t 

Total  Fat 
(g/100gm 
food) 

Red  Meats 

Beef  (average) 

69 

10-15 

Lamb  (average) 

74 

10-15 

Pork  (average) 

63 

10-15 

Veal  (average) 

71 

10 

Organ  meats 

Liver,  beef 

320 

11 

Pancreas  (sweetbreads) 

280 

1 

Kidney 

300 

12 

Brains 

1810 

9 

Poultry 

Chicken  (without  skin) 

light 

54 

5 

dark 

76 

5 

Fish 

Flounder 

50 

3 

Trout,  brook 

57 

3 

Tuna 

51 

3 

Shellfish 

Crab 

99 

1 

Crayfish 

60 

1.5 

Lobster 

83 

1 

Oyster 

59 

2 

Scallop 

51 

2 

Shrimp 

161 

1 

because  these  lower  both  the  LDL  and  HDL  fractions 
of  cholesterol  and  may  increase  the  risk  of  gallstones/ 
it  is  recommended  that  not  more  than  10%  of  dietary 
calories  should  come  from  polyunsaturated  fatty  acids. 
Sources  of  polyunsaturated  fatty  acids  include  plant 
oils  such  as  corn,  sunflower,  soybean,  and  safflower. 
Previously,  monounsaturated  fatty  acids  were  thought 
to  be  neutral  in  their  effect  on  serum  cholesterol;  how- 
ever, recently,  these  fatty  acids,  when  substituted  for 
saturated  fatty  acids  in  the  diet,  have  been  shown  to 
lower  total  cholesterol  by  selectively  lowering  LDL 
fraction.^  Monounsaturated  fatty  acids  are  found  in 
olive  oil,  rapeseed  (canola  oil)  and  other  high-oleic 
forms  of  sunflower  oil. 

Severe  reduction  (less  than  30%  of  calories  as  fat) 


of  total  amount  of  fat  in  the  diet  is  not  necessary  for 
successful  lowering  of  serum  cholesterol  provided 
saturated  fatty  acids  are  reduced.^  For  obese  patients, 
the  decrease  in  total  fat  will  facilitate  weight  reduc- 
tion. 

DIETARY  CHOLESTEROL 

The  second  factor  which  contributes  to  increased 
serum  cholesterol  levels  is  a relatively  high  intake  of 
cholesterol.  The  average  American  diet  contains  ap- 
proximately 350  mg  to  450  mg  of  cholesterol  a day.^ 
Dietary  cholesterol  will  increase  serum  cholesterol 
levels  by  approximately  4 mg/dl  per  100  mg  choles- 
terol.^ Although  all  animal  products  contain  choles- 
terol in  both  the  fat  and  muscle  of  the  animal,  the 
most  concentrated  sources  of  dietary  cholesterol  are 
egg  yolk  and  organ  meats  (liver,  kidney,  sweet- 
breads). Shrimp  contain  a moderate  amount  of  cho- 
lesterol while  other  shellfish  (oysters,  crayfish,  and 
crabs)  contain  considerably  less  (Table  1). 

DIETARY  CALORIES 

The  third  factor  is  caloric  intake  that  exceeds  body 
requirements.  Excessive  caloric  intake  may  result  in 
obesity,  may  lead  to  an  overproduction  of  very  low 
density  lipoprotein  (VLDL)  and  thus,  an  increase  in 
low  density  lipoprotein  (LDL)  levels.^  Obesity  may 
also  lower  the  high  density  lipoprotein  (HDL)  fraction 
of  cholesterol.  Loss  of  body  weight  may  not  only  fa- 
vorably influence  serum  cholesterol  levels  but  may 
also  decrease  triglyceride  levels  in  persons  with  hy- 
pertriglyceridemia . 

DIETARY  THERAPY  OF  HIGH  BLOOD 
CHOLESTEROL  AND  BORDERLINE 
HIGH  CHOLESTEROL 

The  American  Heart  Association  and  National  Cho- 
lesterol Education  Program  have  designed  a two-step 
approach  for  the  modification  of  diet  for  elevated  cho- 
lesterol levels.  This  approach,  outlined  in  Table  2,  is 
designed  to  progressively  reduce  intake  of  saturated 
fatty  acids  and  dietary  cholesterol  and  to  eliminate 
excess  calories,  if  necessary.  The  Step  1 Diet,  as  de- 
scribed below,  is  prescribed  by  the  physician  and  im- 
plemented by  the  physician  and  the  immediate  staff. 
The  patient's  serum  cholesterol  should  be  measured 
at  four  to  six  weeks  and  at  three  months  following 


40  JOURNAL  VOL  140  MAY 


Recommended  Intake 


Nutrient 

Step  1 

Step  2 

Total  fatf 

less  than  30%  of  calories 

less  than  30%  of  calories 

Saturated  fatty  acids 

< 1 0%  of  calories 

<7%  of  calories 

Polyunsaturated  fatty  acids 

up  to  1 0%  of  calories 

up  to  1 0%  of  calories 

Monounsaturated  fatty  acids 

1 0%  to  1 5%  of  calories 

1 0%  to  1 5%  of  calories 

Cabohydrates 

50%  to  60%  of  calories 

50%  to  60%  of  calories 

Protein 

1 0%  to  20%  of  calories 

1 0%  to  20%  of  calories 

Cholesterol 

<300  mg/day 

<200  mg/day 

Total  Calories 

To  achieve  and  maintain 

To  achieve  and  maintain 

desirable  weight 

desirable  weight 

initiation  of  Step  1 . If  there  is  not  sufficient  reduction 
of  serum  cholesterol  at  the  end  of  three  months,  Phase 
2 should  be  initiated  with  the  assistance  of  a registered 
dietitian.  As  noted  in  Table  2,  Phase  2 is  lower  in 
dietary  cholesterol  and  saturated  fatty  acids.  Al- 
though the  response  rate  to  the  diet  is  variable  and 
depends  on  the  previous  diet,  it  has  been  estimated 
that  changing  from  the  typical  American  diet  to  the 
Step  1 diet  will  result  in  an  average  decline  of  30  mg/ 
dl  to  40  mg/dl  in  serum  cholesterol.  Progressing  to 
Step  2 should  result  in  an  additional  decrease  of  15 
mg/dl  in  serum  cholesterol.^ 

EVALUATION  OF  PATIENT'S 
CURRENT  DIET 

An  assessment  of  past  dietary  intake  provides  a foun- 
dation from  which  to  direct  modification  of  a patient's 
eating  behavior.  Evaluation  of  diet  will  allow  the  ed- 
ucator to  focus  on  problem  areas  and  prevent  dupli- 
cation of  current  knowledge.  A recent  report®  indi- 
cated that  while  the  general  US  population  could 
identify  primary  sources  of  polyunsaturated  fatty  acids 
and  saturated  fatty  acids,  only  32%  correctly  re- 
sponded to  the  statement  cholesterol  is  found  in  an- 
imal products.  Questions  which  may  be  of  help  in 
evaluating  the  current  diet  are  summarized  in  Table 
3. 


Frequency  and  type  of  milk  consumed. 

Use  and  frequency  of  high-fat  cuts  of  meat  used  in  preparation 
of  vegetables,  beans,  and  stews. 

Use  and  frequency  of  egg  yolks  and  organ  meats. 

Frequency  and  type  of  cheese  consumed. 

Type  of  fat/oil  used  in  cooking  and  as  spread. 

Frequency  and  selection  of  convenience,  processed,  or  fast  foods. 
Cuts  and  amounts  of  meat  consumed. 


RECOMMENDED  PATTERN  FOR 
STEP  1 DIET  (Table  4) 

Meats,  Poultry,  and  Fish 

Meat  consumption  is  limited  to  6 oz  of  lean  meat  (beef, 
pork,  veal,  and  lamb),  skinless  poultry  and  fish.  Table 
1 lists  fat  and  cholesterol  content  of  these  items.  Lean 
cuts  of  beef  include  lean  ground  beef,  rump  roast, 
and  round  steak.  Severe  reduction  of  red  meat  is  not 
advised,  especially  for  premenopausal  women,  since 
meat  is  rich  in  iron  and  protein.  Use  of  skinless  chicken 
and  turkey  along  with  seafood  is  encouraged.  Finfish 
and  shellfish  contain  varying  amounts  of  cholesterol, 
but  are  low  in  saturated  fats.  The  finfish  caught  in 
temperate  waters  of  Louisiana  are  generally  lowfat  ^ 


JOURNAL  VOL  140  MAY  41 


TABLE  4 

CALORIE-CONTROLLED  MEAL  PATTERNS  FOR  STEP  1 DIET 

2500 

Number  of  Servings 
2000 

1200 

calories 

calories 

calories 

Lean  meats,  poultty,  seafood 

6 oz 

6 oz 

6 oz 

Eggs 

3 per  wk 

3 per  wk 

3 per  wk 

Dairy  Products  (lowfat)* 

3 

3 

2 

Fatt 

8 

7 

3 

Bread,  pasta,  cereal,  starchy  vegetables^ 

8 

7 

3 

Vegetables§ 

5 

5 

4 

Fruitll 

7 

6 

3 

Modified  fat  dessert 

1 

0 

0 

Average  amounts: 

* 8 oz  skim  milk 
t 1 tsp  margarine 
t 1 slice  bread,  3/4  cup  dry  cereal 
§ 1/2  cup  cooked,  1 cup  raw 
11  1/2  cup,  1 raw  fruit 

fish  (excluding  mackerel)  as  compared  to  certain  spe- 
cies found  in  colder  waters.  Shrimp  contain  more  cho- 
lesterol than  other  shellfish;  however,  they  may  be 
included  in  the  diet  by  reducing  the  portion  size  (ie, 
3 oz  lean  meat,  chicken  or  fish  = 2 oz  shrimp).  Some 
foods  to  be  avoided  include  well-marbled  meats  such 
as  rib  eyes,  high  fat  meats  (pickled  pork,  bacon,  etc) 
used  to  flavor  vegetables  and  beans,  commercially 
fried  chicken  and  fish,  and  high  fat  luncheon  meats 
such  as  bologna  and  salami. 

Dairy  Products 

At  least  two  servings  of  low  fat  dairy  products  are 
recommended  for  an  adult  to  maintain  calcium  intake. 
One  serving  is  equal  to  approximately  8 oz  of  skim 
milk,  1 oz  lowfat  cheese  or  1 c of  plain,  lowfat  yogurt. 
Use  skim  milk  or  lowfat  (1%)  milk  as  opposed  to  whole 
milk  which  is  approximately  3.25%  butterfat.  In  ad- 
dition, replace  high  fat  cheeses  (such  as  cheddar, 
Swiss,  blue,  etc)  with  lowfat  cottage  cheese  (1%  to  2% 
butterfat)  and  other  cheeses  made  with  skim  milk, 
such  as  farmer  or  ricotta.  Although  manufacturers 
may  advise  certain  cheeses  as  "lower  in  fat,"  the  ac- 
tual amount  should  be  no  more  than  2 gm  to  6 gm 
fat  per  oz. 

Fats  and  Oils 

Reduce  fats  and  oils  that  are  high  in  saturated  fatty 
42  JOURNAL  VOL  140  MAY 


acids  or  cholesterol.  Generally,  unsaturated  oils  are 
limited  to  six  to  eight  servings  per  day,  but  the  amount 
will  vary  with  the  level  of  calories.  One  serving  is 
equal  to  approximately  1 tsp  of  margarine  or  oil.  De- 
sirable vegetable  oils  include  corn,  cottonseed,  saf- 
flower, rapeseed  (canola),  soybean,  or  olive.  Vege- 
table products  do  not  contain  cholesterol,  but  a high 
intake  will  contribute  excess  calories.  Since  butter  is 
high  in  cholesterol  and  fat,  margarine  is  the  preferred 
spread.  Use  margarines  in  which  the  first  ingredient 
listed  on  the  label  is  a liquid  vegetable  oil,  and  look 
for  partially  hydrogenated  oils  rather  than  hydrogen- 
ated. 

Palm  oil,  palm  kernel  oil,  and  coconut  oil  are  found 
in  many  processed  foods,  bakery  goods,  popcorn  oils, 
and  non-dairy  creamers  and  should  be  avoided  since 
they  are  very  high  in  saturated  fatty  acids. 

The  number  of  egg  yolks  is  limited  to  three  per  week 
including  those  used  in  cooking. 

Breads,  Cereals,  Pasta,  Rice,  Dried  Peas,  and  Beans 
These  products  are  good  sources  of  protein  and  car- 
bohydrate and  most  are  low  in  fat.  At  least  four  serv- 
ings per  day  are  recommended.  One  serving  of  this 
group  is  equal  to  one  slice  of  bread,  two-thirds  to 


three-fourths  cup  of  ready-to-eat  cereal,  or  one-half 
cup  of  cooked  cereal. 

French  bread,  a popular  Louisiana  bread,  con- 
tains little  fat  and  is  appropriate  along  with  sliced, 
hard  rolls,  pita  bread,  English  muffins,  and  bread 
sticks.  Commercially  baked  goods  often  contain 
shortenings  high  in  saturated  fats.  Cornbread,  bis- 
cuits, and  other  quick  breads  may  be  included  in  the 
diet  when  they  are  modified  to  contain  appropriate 
ingredients  (ie,  skim  milk,  margarine,  egg  whites,  or 
egg  substitutes). 

Beans  and  rice,  a mainstay  of  Louisiana  diets,  are 
an  example  of  complimentary  proteins.  Many  people 
will  need  to  adjust  their  cooking  by  deleting  "high 
fat"  seasonings  and  increase  vegetable  seasonings  such 
as  onion,  celery,  and  green  pepper  for  added  flavor. 

Fruits  and  Vegetables 

A minimum  intake  of  three  servings  of  fruits  and  three 
servings  of  vegetables  are  recommended  daily.  A usual 
serving  of  fruit  is  one  medium  size  fruit  or  one-half 
cup  of  canned  fruit,  and  for  vegetables  one-half  cup 
of  cooked  is  considered  an  average  serving.  Com- 
mercially prepared  vegetables  with  cream,  butter,  or 
cheese  sauces  should  be  avoided. 

Alcohol 

Moderate  use  of  alcohol  can  be  included  within  the 
scope  of  the  recommendations,  since  it  does  not  affect 
LDL  concentration.  However,  it  may  increase  serum 
triglyceride  levels  and  HDL-cholesterol  in  some  in- 
dividuals. 

Food  Preparation 

Recommended  methods  include  those  that  require 
little  or  no  fat  in  cooking.  Baking,  steaming,  broiling, 
and  grilling  are  preferred  to  frying.  In  order  to  facil- 
itate change  in  a population  that  often  prefers  frying 
and  stewing  of  their  foods,  recommending  gradual 
modification  may  be  advantageous.  Desirable  vege- 
table oils  should  be  used  on  those  occasions  when 
foods  are  fried.  Reduced  fat  and  appropriate  substi- 
tutions in  stews  and  gumbos  will  allow  patients  to 
still  enjoy  their  foods.  Soups  and  stews  should  be 
chilled  after  cooking,  and  the  congealed  fat  that  forms 
on  top  should  be  removed  prior  to  serving. 

Monitoring 

Follow-up  and  monitoring  are  important  in  order  to 
achieve  a long-term  change  in  eating  behavior.  The 


schedule,  as  proposed  by  the  National  Cholesterol 
Education  Program  and  outlined  in  the  preceding  ar- 
ticle "New  guidelines  for  treatment  of  the  hyper- 
lipidemia in  adults"  (Lopez-SA,  Legardeur  BY),  ad- 
vises that  cholesterol  levels  be  measured  at  four  to  six 
weeks  and  three  months  following  initiation  of  the 
Step  1 diet.  If  the  desired  response  is  achieved,  this 
should  be  confirmed  by  measuring  LDL-cholesterol. 
The  patient  should  then  enter  a long-term  monitoring 
program.  Long-term  monitoring  includes  measuring 
total  cholesterol,  four  times  the  first  year  and  twice 
each  year  thereafter.  Reinforcement  of  the  diet  and 
behavior  is  an  essential  component  of  long-term  mon- 
itoring. When  the  response  to  the  Step  1 diet  is  in- 
adequate, the  person  should  be  referred  to  a regis- 
tered dietitian  for  either  retrial  of  Step  1 diet  or  for 
instruction  on  Step  2 diet.  Cholesterol  levels  should 
be  measured  at  6 and  12  weeks  following  introduction 
of  this  diet.  If  the  desired  cholesterol  level  is  not 
achieved,  drug  therapy  should  be  considered. 

Triglycerides 

The  person  with  borderline  hypertriglyceridemia 
should  be  instructed  to  achieve  and  maintain  ideal 
body  weight.  Since  weight  reduction  diets  (caloricaUy- 
controUed)  are  usually  low  in  fat  and  high  in  carbo- 
hydrate and  this  may  increase  serum  triglyceride  lev- 
els, the  National  Cholesterol  Education  Program  rec- 
ommends that  the  fat  content  not  be  lowered  beyond 
the  Step  1 diet. 

Children 

The  current  recommendations  for  children  over  two 
years  of  age  were  published  by  the  American  Heart 
Association.^  Presently,  guidelines  are  being  devel- 
oped by  a National  Heart,  Lung,  and  Blood  Institute 
Panel  as  part  of  the  National  Cholesterol  Education 
Program. 

Resources 

Educational  materials  are  available  from  the  National 
Cholesterol  Education  Program  and  from  the  Amer- 
ican Heart  Association.  The  Louisiana  affiliate  of  the 
American  Heart  Association  maintains  patient  edu- 
cation materials  in  its  office.  ■ 

REFERENCES 

1.  Report  of  the  expert  panel  on  detection,  evaluation,  and  treatment  of  high 
blood  cholesterol  in  adults.  National  Heart,  Lung,  and  Blood  Institute. 
Arch  Intern  Med  1988;148:36. 


JOURNAL  VOL  140  MAY  45 


2.  Moore  MC,  Guzman  MA,  Schilling  PE,  et  al:  Dietary-artherosderosis  study 

on  deceased  persons.  / Am  Diet  Assoc  1977;70:602. 

3.  Balart  L,  Moore  MC,  Gremillion  L,  et  al:  Serum  lipids,  dietary  intakes 

and  physical  exercise  in  medical  students.  / Am  Diet  Assoc  1974;64:42. 

4.  Dayton  S,  Pearce  ML,  Hashimota  S,  et  al:  A controlled  clinical  trial  of  a 

diet  high  in  unsaturated  fat  in  preventing  complications  of  atheroscle- 
rosis. Circulation  1969;39-40(suppl  2). 

5.  Mattson  FH,  Grundy  SM:  Comparison  of  effect  of  dietary  saturated,  mon- 

ounsaturated,  and  polyunsaturated  fatty  acids  of  lipids  and  lipoproteins 
in  man.  } Lipid  Red  1985;26:194. 

6.  Hegsted  DM:  Serum  cholesterol  response  to  dietary  cholesterol:  A re- 

evaluation.  Am  J Clin  Nutr  1986;44:299. 

7.  Kesardemi  YA,  Grundy  SM:  Increased  low  density  lipoprotein  production 

associated  with  obesity.  Artery  1983;3:170. 

8.  Schucker  B,  Bailey  K,  Heimbach  JT,  et  al:  Change  in  public  perspective 

on  cholesterol  and  heart  disease.  JAMA  1987;258(24):3527. 

9.  Weidman  W,  Kwiterovich  P,  Jesse  MJ,  et  al:  Diet  in  the  healthy  child. 

AHA  Committee  Report.  Circulation  1983;67:1411A. 

10.  Connor  WF,  Cormor  SL:  Dietary  treatment  of  hyperlipidemia,  in  Hyper- 
lipidemia, Rifkind  B,  Levy  R (eds).  New  York,  Grune  & Stratton,  1977: 
p 297. 


Ms  Legardeur  is  an  assistant  professor  of  clinical  medicine  from  the 
Dept  of  Medicine,  Nutrition  Section,  at  LSU  School  of  Medicine  in 

New  Orleans. 

Dr  Lopez-S  is  a professor  of  medicine  in  the  Dept  of  Medicine, 
Nutrition  Section,  at  LSU  School  of  Medicine  in  New  Orleans. 

Reprints  will  not  be  available. 


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46  JOURNAL  VOL  140  MAY 


PHARMACOLOGIC  TREATMENT  OF 
HYPERCHOLESTEROLEMIA 


STEVEN  N.  LEVINE,  MD 


Pharmacologic  therapy  for  hypercholesterolemia  is 
indicated  for  those  individuals  with  significant 
elevations  of  the  serum  cholesterol  following  an 
adequate  trial  of  dietary  modification.  Initiation  of 
drug  therapy  is  recommended  for  patients  without 
a history  of  coronary  heart  disease  or  other  risk 
factors  if  low  density  lipoprotein  (LDL)-cholesterol 
levels  are  ^ 190  mg/dl  following  at  least  six 
months  of  adherence  to  a cholesterol  lowering  diet. 
An  LDL-cholesterol  value  of  ^ 160  mg/dl  is  used 
as  a cutoff  for  those  patients  with  coronary  heart 
disease  or  coronary  risk  factors.  This  article 
provides  information  on  the  current  drugs 
available  to  manage  patients  with 
hypercholesterolemia,  including  lovastatin,  an 
agent  recently  approved  for  clinical  use.  For  each 
drug  a summary  of  the  indicatioins,  expected 
response,  potential  side  effects,  and  recommended 

dosage  is  provided. 


Epidemiological  data,  supported  by  animal  and 
genetic  investigations,  provide  conclusive  evi- 
dence for  a causal  relationship  between  serum  cho- 
lesterol levels  and  the  incidence  of  coronary  heart 
diseased  Furthermore,  clinical  trials  such  as  the  Lipid 
Research  Clinic-Coronary  Primary  Prevention  Trial 
demonstrate  that  lowering  of  serum  cholesterol  levels 
reduces  the  frequency  of  fatal  and  nonfatal  myocar- 
dial infarctions  d Therefore,  few  would  disagree  with 
recommendations  to  reduce  cholesterol  levels  in 
Western  populations  as  a whole,  and  to  specifically 
lower  cholesterol  levels  in  patients  with  significant 
elevations  of  total  and  low  density  lipoprotein  (LDL)- 
cholesterol. 

This  review  focuses  on  the  pharmacologic  man- 
agement of  primary  hypercholesterolemia.  Other  ar- 
ticles in  this  issue  deal  with  the  evaluation  and  dietary 
therapy  of  this  group  of  disorders.  However,  several 
points  deserve  emphasis.  First,  other  etiologies  of  hy- 
percholesterolemia, such  as  hypothyroidism  must  be 
excluded  before  identifying  and  treating  an  individual 
for  primary  hypercholesterolemia.  Obviously,  such 
patients  are  treated  in  quite  a different  manner  than 
those  with  primary  disorders  of  cholesterol  metabo- 
lism. Second,  most  individuals  with  hypercholester- 
olemia can  effectively  be  managed  with  dietary  mod- 


JOURNAL  VOL  140  MAY  47 


TABLE 

RECOMMENDED  LDL-CHOLESTEROL  LEVELS  FOR 
INITIATING  DRUG  THERAPY  FOLLOWING  AN  ADEQUATE 
TRIAL  OF  DIET 


LDL-cholesterol  > 1 90  mg/dl  — without  definite  CHD  or  two  other 
CHD  risk  factors 

LDL-cholesterol  > 1 60  mg/dl  — with  a history  of  definite  CHD  or 
two  other  CHD  risk  factors. 

CHD  risk  factors 
Male  sex 

Family  history  of  premature  CHD 
Cigarette  smoking 
Hypertension 

Low  HDL-cholesterol  (<  35  mg/dl) 

Diabetes  mellitus 

History  of  cerebrovascular  or  peripheral  vascular  disease 
Severe  obesity  (>  30%  overweight) 


CHD  = coronary  heart  disease 


ifications,  avoiding  the  need  for  long-term  drug 
administration.  Third,  hypercholesterolemia  repre- 
sents only  one  of  several  identified  risk  factors  for 
coronary  heart  disease.  While  treating  the  elevated 
cholesterol,  patients  need  to  be  counseled  to  reduce 
other  risk  factors,  such  as  smoking. 

The  recently  released  report  from  the  National 
Cholesterol  Education  Program  provides  specific  rec- 
ommendations and  guidelines  for  initiating  dietary 
and  pharmacologic  therapy  for  hypercholesterol- 
emia.^ Addition  of  drugs  is  recommended  for  those 
patients  who,  following  a minimum  of  six  months  of 
strict  dietary  treatment,  have  persistent  elevations  of 
LDL-cholesterol.  The  goal  of  therapy  is  to  maximally 
reduce  LDL-cholesterol  levels  with  agents  such  as  bile 
salt  sequestrants  and  nicotinic  acid.  Recently,  ap- 
proval by  the  Food  and  Drug  Administration  of  lo- 
vastatin,  an  inhibitor  of  cholesterol  synthesis,  has  pro- 
vided clinicians  with  a new  class  of  drug  to  reduce 
serum  cholesterol  concentrations.  Pharmacologic  in- 
tervention to  raise  high  density  lipoprotein  (HDL)- 
cholesterol  levels  represents  an  additional  approach 
to  reducing  coronary  heart  disease.  A recent  report 
from  the  Helsinki  Heart  Stud)^  demonstrated  a re- 
duced rate  of  cardiac  events  in  hyperlipidemic  males 
treated  with  gemfibrozil,  an  agent  principally  utilized 
to  lower  triglyceride  levels,  but  having  the  added  ben- 
efit of  raising  HDL-cholesterol  concentrations. 

For  those  individuals  without  a history  of  coro- 


nary heart  disease  or  two  other  coronary  heart  disease 
risk  factors,  drug  therapy  is  recommended  if  LDL- 
cholesterol  levels  equal  or  exceed  190  mg/dl  following 
at  least  six  months  of  adherence  to  a cholesterol  low- 
ering diet.  An  LDL-cholesterol  value  of  ^ 160  mg/dl 
is  used  as  a cutoff  for  those  patients  with  definite 
coronary  heart  disease  or  two  risk  factors  (Table). ^ The 
goal  of  drug  therapy  is  reduction  of  LDL-cholesterol 
to  < 160  mg/dl  for  those  without  coronary  heart  dis- 
ease or  risk  factors  and  < 130  mg/dl  for  patients  with 
a history  of,  or  at  greater  risk  for,  coronary  heart  dis- 
ease. 

BILE  SALT  SEQUESTRANTS 

The  bile  salt  sequestrants  cholestyramine  and  coles- 
tipol are  considered  first  line  drugs  for  management 
of  hypercholesterolemia.^  They  have  clearly  been 
demonstrated  to  reduce  LDL-cholesterol  levels,  while 
having  minimal  systemic  toxicity  since  they  are  not 
absorbed  from  the  gastrointestinal  tract.  Both  drugs, 
being  anionic  binding  resins,  bind  bile  salts,  reducing 
their  resorption  from  the  terminal  ileum,  interrupting 
the  enterohepatic  circulation. ^ The  resulting  reduc- 
tion in  the  size  of  the  bile  salt  pool  stimulates  hepatic 
conversion  of  cholesterol  to  bile  acids,  increasing  the 
liver's  demand  for  cholesterol.  As  a consequence,  he- 
patic synthesis  of  cholesterol  increases,  as  does 
expression  of  high  affinity  LDL  receptors  on  the  cell 
surface.^  Increased  cholesterol  clearance  via  hepatic 
LDL  receptors  is  partially  offset  by  increased  hepatic 
cholesterol  synthesis,  but  the  net  effect  is  a 15%  to 
30%  reduction  in  circulating  LDL-cholesterol  levels. 
Concomitant  administration  of  an  hydroxymethyl- 
glutaryl  (HMG)  CoA  reductase  inhibitor  such  as  lo- 
vastatin,  significantly  reduces  the  compensatory  in- 
crease in  hepatic  cholesterol  synthesis,  potentiating 
the  hypocholesterolemic  effect  of  the  bile  salts  se- 
questrants. 

Administration  of  bile  salt  sequestrants  lowers 
cholesterol  in  patients  with  a variety  of  etiologies  of 
primary  hypercholesterolemia,  including  heterozy- 
gotes for  familial  hypercholesterolemia.  These  indi- 
viduals express  only  50%  of  the  normal  quantity  of 
functional  LDL  receptors  on  cell  membranes.  The 
administration  of  drugs  that  increase  the  number  of 
LDL  receptors  partially  corrects  the  underlying  path- 
ophysiologic defect.^  Unfortunately  these  drugs  (as 
well  as  HMG  CoA  reductase  inhibitors)  provide  no 
beneficial  effect  in  homozygotes  for  familial  hyper- 


48  JOURNAL  VOL  140  MAY 


cholesterolemia  who  lack  the  ability  to  express  any 
functional  LDL  receptors. 

Cholestyrarnine  is  available  in  packets  (5  g of  drug 
+ 4 g of  flavored  filler)  or  bulk  containers.  Similarly, 
colestipol  can  be  purchased  in  5 g packets  or  bulk. 
Both  are  granular  powders  that  must  be  mixed  with 
water,  juice,  carbonated  beverages,  or  foods  such  as 
applesauce.  As  noted  above,  the  bile  salt  sequestrants 
are  not  absorbed  from  the  gastrointestinal  tract  and 
thus  systemic  toxicity  is  minimal.  However,  gastroin- 
testinal complaints  including  constipation,  bloating, 
nausea,  and  flatulence  are  common.  Constipation  can 
usually  be  managed  by  increasing  dietary  fiber  or  ad- 
dition of  a bulk  laxative.  Caution  must  be  exercised 
in  administering  bile  salt  sequestrants  with  other 
medications,  as  the  resins  may  bind  a variety  of  drugs 
including  thyroxine,  digitalis  compounds,  thiazide  di- 
uretics, phenylbutazone,  beta  blockers,  phenobarbi- 
tal,  and  warfarin.  It  is  therefore  advisable  to  admin- 
ister other  medications  at  least  one  hour  before,  or 
four  hours  following,  cholestyramine  or  colestipol.^'  ^ 
Furthermore,  large  doses,  particularly  in  patients  with 
hepatic  or  small  bowel  disease,  may  result  in  de- 
creased absorption  of  fat  soluble  vitamins.  However, 
routine  administration  of  vitamins  is  usually  not  nec- 
essary in  adults.  The  bile  salt  sequestrants  tend  to 
cause  modest  elevations  in  serum  triglyceride  and  are 
best  avoided  as  single  agents  in  hypercholesterolemic 
patients  with  concomitant  triglyceride  levels  > 500 
mg/dl.^ 


Most 
patients 
need 
only  one. 


NICOTINIC  ACID 

Nicotinic  acid  has  long  been  recognized  as  a hypo- 
lipidemic agent  whose  primary  action  is  to  reduce 
hepatic  very  low  density  lipoprotein  (VLDL)  synthe- 
sis. Because  VLDL  serve  as  precursors  for  LDL  pro- 
duction, the  serum  concentrations  of  both  lipopro- 
teins decrease  when  pharmacologic  doses  of  nicotinic 
acid  are  administered.^  LDL-cholesterol  typically  de- 
creases 15%  to  25%,  often  accompanied  by  an  increase 
in  HDL-cholesterol.  This  drug  is  considered  a first  line 
agent  for  managing  patients  with  hypercholestero- 
lemia and  generally  considered  the  drug  of  choice  for 
patients  with  familial  combined  hyperlipidemia.^ 
Nicotinic  acid,  while  quite  efficacious,  must  be 
administered  cautiously  due  to  its  wide  spectrum  of 
toxic  effects.  Prostaglandin-mediated  cutaneous 
flushing  is  a common  complaint  that  can  be  reduced 
by  pretreatment  with  aspirin  or  other  nonsteroidal  ► 


K-»UR20 

(potassium  chloride)  20mEq 


Microburst 

Release 

System" 

Sustained  Release 
Tablets 


A daily  prophylactic  dose 
in  a single  tablet. 

Please  see  next  page  for  brief  summary  of  prescribing  information. 


Pharmaceuticals,  Inc. 
Kenilworth,  NJ  07033 

World  leader  in  drug  delivery  systems. 


Copyright  © 1987,  Key  Pharmaceuticals,  Inc.,  Kenilworth,  NJ  07033. 
All  rights  reserved.  KD-2055/14238603H  8/87 


K-9UK 

(potassium  chloride) 


Microburst 

Release 

System" 

Sustaned  Release  Tablets 


INDICATIONS  AND  USAGE:  BECAUSE  OF  REPORTS  OF  INTESTINAL  AND  GASTRIC  ULCERATION  AND 
BLEEDING  WITH  SLOW-RELEASE  POTASSIUM  CHLORIDE  PREPARATIONS,  THESE  DRUGS  SHOULD 
BE  RESERVED  FOR  THOSE  PATIENTS  WHO  CANNOT  TOLERATE  OR  REFUSE  TO  TAKE  LIQUID  OR  EF- 
FERVESCENT POTASSIUM  PREPARATIONS  OR  FOR  PATIENTS  IN  WHOM  THERE  IS  A PROBLEM  OF 
COMPLIANCE  WITH  THESE  PREPARATIONS. 

1.  For  therapeutic  use  In  patients  with  hypokalemia  with  or  without  metabolic  alkalosis,  in  digitaiis 
intoxication  and  in  patients  with  hypokalemic  familial  periodic  paralysis. 

2.  For  the  prevention  of  potassium  depletion  when  the  dietary  intake  is  inadequate  in  the  following 
conditions:  Patients  receiving  digitalis  and  diuretics  for  congestive  heart  failure,  hepatic  cirrhosis 
with  ascites,  states  of  aldosterone  excess  with  normal  renal  function,  potassium-losing  nephropathy, 
and  with  certain  diarrheai  states. 

3.  The  use  of  potassium  salts  in  patients  receiving  diuretics  for  uncomplicated  essential  hyperten- 
sion is  often  unnecessary  when  such  patients  have  a normal  dietary  pattern.  Serum  potassium 
should  be  checked  periodically,  however,  and  if  hypokalemia  occurs,  dietary  supplementation  with 
potassium-containing  foods  may  be  adequate  to  control  milder  cases.  In  more  severe  cases  sup- 
plementation with  potassium  salts  may  be  indicated. 

CONTRAINDICATIONS:  Potassium  supplements  are  contraindicated  in  patients  with  hyperkalemia 
since  a further  increase  in  serum  potassium  concentration  in  such  patients  can  produce  cardiac 
arrest.  Hyperkalemia  may  complicate  any  of  the  following  conditions:  Chronic  renal  failure,  systemic 
acidosis  such  as  diabetic  acidosis,  acute  dehydration,  extensive  tissue  breakdown  as  in  severe  burns, 
adrenal  insufficiency,  or  the  administration  of  a potassium-sparing  diuretic  (e.g.,  spironolactone, 
triamterene). 

Wax-matrix  potassium  chloride  preparations  have  produced  esophageal  ulceration  in  certain  cardi- 
ac patients  with  esophageal  compression  due  to  enlarged  left  atrium. 

All  solid  dosage  forms  of  potassium  chloride  supplements  are  contraindicated  in  any  patient  in 
whom  there  is  cause  for  arrest  or  delay  in  tablet  passage  through  the  gastrointestinal  tract.  In  these 
instances,  potassium  supplementation  should  be  with  a liquid  preparation. 

WARNINGS:  Hyperkalemia— In  patients  with  impaired  mechanisms  for  excreting  potassium,  the  ad- 
ministration of  potassium  salts  can  produce  hyperkalemia  and  cardiac  arrest.  This  occurs  most  com- 
monly in  patients  given  potassium  by  the  intravenous  route  but  may  also  occur  in  patients  given 
potassium  orally.  Potentially  fatal  hyperkalemia  can  develop  rapidly  and  be  asymptomatic.  The  use  of 
potassium  salts  in  patients  with  chronic  renal  disease,  or  any  other  condition  which  impairs  potas- 
sium excretion,  requires  particularly  careful  monitoring  of  the  serum  potassium  concentration  and 
appropriate  dosage  adjustment. 

Interaction  with  Potassium  Sparing  Diuretics— Hypokalemia  should  not  be  treated  by  the  con- 
comitant administration  of  potassium  salts  and  a potassium-sparing  diuretic  (e.g.,  spironolactone  or 
triamterene)  since  the  simultaneous  administration  of  these  agents  can  produce  severe  hyperkalemia. 

Gastrointestinal  Lesions— Potassium  chloride  tablets  have  produced  stenotic  and/or  ulcerative 
lesions  of  the  small  bowel  and  deaths.  These  lesions  are  caused  by  a high  localized  concentration  of 
potassium  ion  in  the  region  of  a rapidly  dissolving  tablet,  which  injures  the  bowel  wall  and  thereby 
produces  obstruction,  hemorrhage  or  perforation. 

K-DUR  tablets  contain  micro-crystalloids  which  disperse  upon  disintegration  of  the  tablet.  These 
micro-crystalloids  are  formulated  to  provide  a controlled  release  of  potassium  chloride.  The  dispersi- 
bility of  the  micro-crystalloids  and  the  controlled  release  of  ions  from  them  are  intended  to  minimize 
the  possibility  of  a high  local  concentration  near  the.gastrointestinal  mucosa  and  the  ability  of  the  KOI 
to  cause  stenosis  or  ulceration.  Other  means  of  accomplishing  this  (e.g.,  incorporation  of  potassium 
chloride  into  a wax  matrix)  have  reduced  the  frequency  of  such  lesions  to  less  than  one  per  100,000 
patient  years  (compared  to  40-50  per  100,000  patient  years  with  enteric-coated  potassium  chloride) 
but  have  not  eliminated  them.  The  frequency  of  Gl  lesions  with  K-DUR  tablets  is,  at  present, 
unknown.  K-DUR  tablets  should  be  discontinued  immediately  and  the  possibility  of  bowel  obstruction 
or  perforation  considered  if  severe  vomiting,  abdominal  pain,  distention,  or  gastrointestinal  bleeding 
occurs. 

Metabolic  Acidosis— Hypokalemia  in  patients  with  metabolic  acidosis  should  be  treated  with  an 
alkalinizing  potassium  salt  such  as  potassium  bicarbonate,  potassium  citrate,  potassium  acetate,  or 
potassium  gluconate. 

PRECAUTIONS:  The  diagnosis  of  potassium  depletion  is  ordinarily  made  by  demonstrating  hypokale- 
mia in  a patient  with  a clinical  history  suggesting  some  cause  for  potassium  depletion.  In  interpreting 
the  serum  potassium  level,  the  physician  should  bear  in  mind  that  acute  alkalosis  per  se  can  produce 
hypokalemia  in  the  absence  of  a deficit  in  total  body  potassium  while  acute  acidosis  per  se  can  in- 
crease the  serum  potassium  cohcentration  into  the  normal  range  even  in  the  presence  of  a reduced 
total  body  potassium.  The  treatment  of  potassium  depletion,  particularly  in  the  presence  of  cardiac 
disease,  renal  disease,  or  acidosis  requires  careful  attention  to  acid-base  balance  and  appropriate 
monitoring  of  serum  electrolytes,  the  electrocardiogram,  and  the  clinical  status  of  the  patient. 

Laboratory  Tests:  Regular  serum  potassium  determinations  are  recommended.  In  addition,  during 
the  treatment  of  potassium  depletion,  careful  attention  should  be  paid  to  acid-base  balance,  other 
serum  electrolyte  levels,  the  electrocardiogram,  and  the  clinical  status  of  the  patient,  particularly  in 
the  presence  of  cardiac  disease,  renal  disease,  or  acidosis. 

Drug  Interactions:  Potassium-sparing  diuretics;  see  WARNINGS. 

Carcinogenesis,  Mutagenesis,  Impairment  of  Fertility:  Long-term  carcinogenicity  studies  in 
animals  have  not  been  performed. 

Pregnancy  Category  C:  Animal  reproduction  studies  have  not  been  conducted  with  K-DUR.  It  is 
also  not  known  whether  K-DUR  can  cause  fetal  harm  when  administered  to  a pregnant  wqman  or  can 
affect  reproduction  capacity,  K-DUR  should  be  given  to  a pregnant  woman  only  if  clearly  needed. 

Nursing  Mothers:  The  normal  potassium  ion  content  of  human  milk  is  about  13  mEq  per  liter.  Since 
oral  potassium  becomes  part  of  the  body  potassium  pool,  so  long  as  body  potassium  is  not  exces- 
sive, the  contribution  of  potassium  chloride  supplementation  should  have  little  or  no  effect  on  the 
level  in  human  milk. 

Pediatric  Use:  Safety  and  effectiveness  in  children  have  not  been  established. 

ADVERSE  REACTIONS:  One  of  the  most  severe  adverse  effects  is  hyperkalemia  (see  CONTRAINDICATIONS, 
WARNINGS,  and  OVERDOSAGE).  There  have  also  been  reports  of  upper  and  lower  gastrointestinal 
conditions  including  obstruction,  bleeding,  ulceration,  and  perforation  (see  CONTRAINDICATIONS 
and  WARNINGS):  other  factors  known  to  be  associated  with  such  conditions  were  present  in  many  of 
these  patients. 

The  most  common  adverse  reactions  to  oral  potassium  salts  are  nausea,  vomiting,  abdominal  dis- 
comfort, and  diarrhea.  These  symptoms  are  due  to  irritation  of  the  gastrointestinal  tract  and  are  best 
managed  by  taking  the  dose  with  meals  or  reducing  the  dose. 

Skin  rash  has  been  reported  rarely. 

OVERDOSAGE:  The  administration  of  oral  potassium  salts  to  persons  with  normal  excretory  mecha- 
nisms for  potassium  rarely  causes  serious  hyperkalemia.  However,  if  excretory  mechanisms  are  im- 
paired or  if  potassium  is  administered  too  rapidly  intravenously,  potentially  fatal  hyperkalemia  can 
result  (see  CONTRAINDICATIONS  and  WARNINGS),  It  is  important  to  recognize  that  hyperkalemia  is 
usually  asymptomatic  and  may  be  manifested  only  by  an  increased  serum  potassium  concentration 
and  characteristic  electrocardiographic  changes  (peaking  of  T-waves,  loss  of  P-waves,  depression  of 
S-T  segment,  and  prolongation  of  the  QT-interval).  Late  manifestations  include  muscle-paralysis  and 
cardiovascular  collapse  from  cardiac  arrest. 

Treatment  measures  for  hyperkalemia  include  the  following: 

1.  Elimination  of  foods  and  medications  containing  potassium  and  of  potassium-sparing  diuretics. 

2.  Intravenous  administration  of  300  to  500  ml/hr  of  10%  dextrose  solution  containing  10-20  units 
of  insulin  per  1,000  ml. 

3.  Correction  of  acidosis,  if  present,  with  intravenous  sodium  bicarbonate. 

4.  Use  of  exchange  resins,  hemodialysis,  or  peritoneal  dialysis. 

In  treating  hyperkalemia,  it  should  be  recalled  that  in  patients  who  have  been  stabilized  on 
digitalis,  too  rapid  a lowering  of  the  serum  potassium  concentration  can  produce  digitalis  toxicity. 


1002004 


##"■#  Key  Pharmaceuticals,  Inc. 

Kenilworth,  NJ  07033  (USA) 

World  leader  in  drug  delivery  systems. 


13944326 
Rev.  4/87 


anti-inflammatory  agents.  Tolerance  to  this  side  effect 
usually  develops  and  symptoms  can  be  limited  by 
slowly  titrating  the  dose  of  nicotinic  acid  upward. 
However,  if  doses  are  omitted  the  flushing  tends  to 
worsen,  and  thus  education  concerning  proper  • 
administration  is  essential  if  patient  compliance  is  ex-  ■ 
pected.  Abdominal  discomfort,  diarrhea,  as  well  as 
flushing,  can  be  limited  by  administering  the  drug 
with  food.  Additional  side  effects  include  hepatic  dys- 
hmction,  hyperuricemia,  glucose  intolerance,  dry  skin, 
increased  skin  pigmentation  with  acanthosis  nigri- 
cans, cardiac  arrhythmias,  and  activation  of  peptic 
ulcer  disease.  Nicotinic  acid  is  contraindicated  in  pa-  I 
tients  with  hepatic  disease,  gout,  significant  hyper- 
uricemia, peptic  ulcer  disease,  or  significant  cardiac  , 
arrhythmias,  and  should  be  used  with  caution  in  pa-  j 
tients  with  diabetes  mellitus.  Liver  function  tests,  glu-  , i 
cose,  and  uric  acid  should  be  monitored  periodically  ! ; 
in  patients  treated  with  this  drug.  ! 

Nicotinic  acid  therapy  is  initiated  at  a low  dose,  ‘ j 
100  mg  one  to  three  times/day  with  meals.  The  dose  | 
is  slowly  titrated  upward  every  four  to  seven  days, 
depending  on  individual  tolerance  to  side  effects,  par- 
ticularly flushing.  Since  toxic  reactions  to  nicotinic 
acid  tend  to  occur  at  higher  doses,  it  is  recommended 
that  the  therapeutic  response  be  measured  once  the 
dose  has  reached  2 g per  day.  If  a satisfactory  lowering 
of  LDL-cholesterol  has  not  been  achieved  at  this  lower 

I 

dose,  an  increase  to  3 g per  day  is  recommended.  j 
Further  increases  up  to  6 g per  day  are  occasionally  ; 
necessary  to  achieve  the  desired  response. ^ 

Nicotinic  acid  has  proved  to  be  particularly  ef- 
fective in  lowering  cholesterol  when  used  in  combi- 
nation with  cholestyramine  or  colestipol.  Patients  with 
significant  hypercholesterolemia  able  to  tolerate  full 
therapeutic  doses  of  both  drugs  can  commonly  achieve 
normal  LDL-cholesterol  levels.® 

HMG  CoA  REDUCTASE  INHIBITORS 

The  discovery  of  fungal  metabolites  that  competitively 
inhibit  HMG  CoA  reductase,  the  rate  limiting  enzyme 
in  cholesterol  synthesis,  provides  clinicians  with  a 
new  class  of  pharmacologic  agent  to  manage  hyper- 
cholesterolemia. Lovastatin  (formerly  referred  to  as 
mevinolin)  is  the  first  such  agent  approved  for  use  by 
the  Food  and  Drug  Administration.  Increased  syn- 
thesis of  HMG  CoA  reductase  partially  compensates 
for  reduced  hepatic  cholesterol  synthesis.  However, 
reduced  cholesterol  synthesis  causes  increased  num- 


bers  of  LDL-receptors  on  hepatic  membranes,  low- 
ering LDL  levels  by  increasing  receptor-mediated  ca- 
tabolism of  this  lipoprotein/  Additional  data  suggests 
that  lovastatin  also  results  in  a modest  decrease  in 
LDL  production. 

Used  as  a single  agent,  lovastatin  typically  lowers 
total  cholesterol  levels  by  20%  to  35%,  LDL-choles- 
terol  levels  by  25%  to  45%,  and  increases  HDL-cho- 
lesterol  concentrations  6%  to  10%  in  individuals  with 
both  nonfamilial  hypercholesterolemia  and  hetero- 
zygotes for  familial  hypercholesterolemia.^'  Com- 
bined therapy  with  bile  salt  sequestrants  and  lova- 
statin lowers  cholesterol  levels  to  a greater  degree 
than  either  agent  alone.  This  combination  of  drugs  is 
particularly  attractive  since  lovastatin  blocks  the  com- 
pensatory increase  in  cholesterol  synthesis  that  occurs 
when  a bile  salt  sequestrant  is  used  alone. ^ As  a con- 
sequence, an  even  greater  number  of  LDL-receptors 
are  expressed,  further  increasing  receptor-mediated 
LDL  uptake  and  catabolism  (Fig  1).  Combined  ther- 
apy can  result  in  reductions  of  LDL-cholesterol  of  up 
to  60%.  Unfortunately,  lovastatin  is  not  beneficial  in 
the  treatment  of  homozygotes  for  familial  hypercho- 
lesterolemia, since  such  patients  cannot  express  any 
functional  LDL-receptors.  An  exception  has  been  a 
patient  treated  by  liver  transplantation  (providing  a 
source  of  LDL-receptors)  followed  by  lovastatin  ther- 
apy.7 

Lovastatin  is  generally  well-tolerated.  Occasional 
patients  have  reported  abnormalities  in  bowel  func- 
tion, headaches,  or  pruritus  that  usually  do  not  re- 
quire discontinuation  of  therapy.  Infrequently  the  drug 
may  cause  myositis  with  increases  in  creatine  phos- 
phokinase  (CPK),  and  rarely  rhabdomyolysis.  Pa- 
tients on  lovastatin  must  have  liver  function  tests 
monitored  at  frequent  intervals  (every  four  to  six  weeks 
for  15  months)  since  up  to  1.9%  of  treated  patients 
develop  persistent  elevations  of  transaminase  levels 
that  require  discontinuation  of  the  drug.  An  addi- 
tional concern  is  the  possible  association  of  lovastatin 
with  the  development  of  lens  opacifications.  There- 
fore, patients  should  have  an  initial  and  annual  slit 
lamp  examination.^ 

Recommended  doses  are  between  20  mg/day  to 
80  mg/day.  Therapy  is  initiated  at  a dose  of  20  mg 
with  the  evening  meal,  although  an  initial  dose  of  20 
mg  twice  a day  may  be  chosen  for  patients  with  severe 
hypercholesterolemia  (cholesterol  >300  mg/dl).  The 
maximal  hypocholesterolemic  response  to  a particular 
dose  is  typically  obtained  by  four  weeks  of  therapy 


and  thus  increases  in  dosage  should  not  be  made 
more  frequently  than  monthly.  Patients  do  not  de- 
velop tolerance  to  the  cholesterol-lowering  effects  of 
lovastatin;  the  beneficial  response  persists  as  long  as 
the  drug  is  continued.^-  Since  cholesterol  serves  as 
a precursor  for  steroid  hormone  biosynthesis,  phar- 
macologic agents  that  inhibit  cholesterol  production 
might  potentially  result  in  adrenal  or  gonadal  steroid 
hormone  deficiencies.  However,  studies  of  endocrine 
function  in  patients  treated  with  lovastatin  have  failed 
to  demonstrate  any  evidence  of  such  deficiencies.^^ 

Lovastatin,  as  well  as  newer  analogs  that  are  un- 
der investigation,  are  potent  hypocholesterolemic 
agents  representing  a significant  advance  in  the  treat- 
ment of  hypercholesterolemia.  However,  enthusiasm 
for  their  administration  must  be  tempered  until  long- 
term safety  has  been  adequately  determined.^ 

PROBUCOL 

Probucol  is  a fat  soluble  compound  that  lowers  serum 
cholesterol  concentrations  by  a mechanism  that  stiU 
remains  incompletely  characterized.  The  drug  in- 
creases the  fractional  catabolic  rate  of  LDL  and  may 
increase  clearance  by  a mechanism  independent  of 
the  high  affinity  LDL-receptor.  A pharmacologic  dose 
of  probucol  typically  lowers  LDL-cholesterol  concen- 
trations 10%  to  15%  but  at  the  same  time  has  the 
disturbing  property  of  reducing  HDL-cholesterol  by 
as  much  as  25%.^ 

The  drug  is  usually  weU  tolerated  with  few  side 
effects.  Diarrhea,  abdominal  pain,  nausea,  and  flat- 
ulence are  occasionally  noted,  but  often  transient,  not 
requiring  discontinuation  of  therapy.  Probucol  can 
prolong  the  QT  interval  and  is  arrhythmogenic  in  ex- 
perimental animals,  although  no  increased  frequency 
of  cardiac  arrhythmias  has  been  noted  in  humans. 
However,  it  should  be  used  with  extreme  caution,  or 
not  at  all,  in  patients  with  prolonged  QT  intervals  or 
clinical  evidence  of  myocardial  irritability.^ 

The  usual  dose  is  500  mg  twice  a day.  Due  to  its 
lipid  solubiLity,  serum  concentrations  decrease  slowly 
following  discontinuation  of  therapy.  Concern  over 
the  reduction  in  HDL-cholesterol  levels  produced  by 
probucol  has  generally  led  physicians  to  restrict  its 
use  to  hypercholesterolemic  patients  who  are  intol- 
erant of  other  modalities  of  therapy. 

CLOFIBRATE 

Clofibrate,  a fibric  acid  derivative,  is  a hypolipidemic  ► 


JOURNAL  VOL  140  MAY  51 


agent  mainly  used  to  lower  serum  triglyceride  levels 
in  patients  at  risk  for  developing  pancreatitis.  Its  prin- 
cipal action  is  to  enhance  removal  of  triglyceride-rich 
lipoproteins  by  increasing  the  activity  of  lipoprotein 
lipase.^  LDL-cholesterol  levels  are  only  slightly  re- 
duced, Clofibrate  increases  biliary  excretion  of  neutral 
sterols,  increasing  the  lithogenicity  of  bile  and  the 
incidence  of  cholelithiasis.  Other  side  effects  include 
nausea,  abdominal  discomfort,  decreased  libido,  and 
transient  abnormalities  in  liver  function.  Myositis  as- 
sociated with  increased  levels  of  CPK  may  occur,  par- 
ticularly in  patients  with  renal  insufficiency.  The  drug 
also  potentiates  the  action  of  coumadin  and  should 
be  used  with  caution  in  patients  receiving  oral  anti- 
coagulants. A concern  of  long-term  safety  was  raised 
by  a World  Health  Organization  study  in  which  pa- 
tients treated  with  clofibrate  experienced  an  increased 
incidence  of  noncardiac  deaths  mainly  due  to  a greater 
number  of  malignancies.^ 

The  usual  dose  of  clofibrate  is  1 g twice  daily.  It 
is  particularly  efficacious  in  the  management  of  pa- 
tients with  dysbetalipoproteinemia  who  have  ele- 
vated concentrations  of  beta-VLDL,  It  is  also  benefi- 
cial for  treatment  of  patients  with  significant  elevations 
of  serum  triglyceride  at  risk  for  developing  pancrea- 
titis, but  has  a very  limited  role  for  use  in  patients 
with  elevated  concentrations  of  LDL-cholesterol. 

GEMFIBROZIL 

The  principal  use  of  gemfibrozil,  another  fibric  acid 
derivative  similar  in  structure  to  clofibrate,  is  to  lower 
the  triglyceride  concentration.  The  drug  has  variable 
effects  on  LDL-cholesterol,  but  can  reduce  its  con- 
centration in  patients  without  significant  hypertri- 
glyceridemia. Gemfibrozil  has  the  added  benefit  of 
raising  HDL-cholesterol  concentrations  by  10%  to 
15%.^  The  drug,  like  clofibrate,  increases  lipoprotein 
lipase  activity  but  has  an  additional  effect  of  reducing 
VLDL  synthesis.  The  spectrum  of  side  effects  is  sim- 
ilar to  clofibrate,  although  gemfibrozil  seems  less  Ukely 
to  cause  cholelithiasis.^ 

The  recent  publication  of  the  Helsinki  Heart  Study 
provided  evidence  that  administration  of  gemfibrozil 
to  patients  with  elevated  non  HDL-cholesterol  levels 
can  reduce  the  incidence  of  coronary  heart  disease.^ 
Compared  to  placebo  treated  subjects,  those  receiving 
gemfibrozil  (600  mg  twice  daily  for  five  years)  had  a 
7%  to  9%  decrease  in  total  cholesterol,  8%  to  9%  de- 
crease in  LDL-cholesterol,  30%  to  40%  decrease  in 


triglyceride,  and  8%  to  10%  increase  in  HDL-choles- 
terol. Treated  patients  had  a 34%  reduction  in  coro- 
nary heart  disease  end  points  (fatal  or  nonfatal  my- 
ocardial infarction  and  cardiac  death).  A modest 
increase  in  gastrointestinal  symptoms  occurred  in  the 
gemfibrozil  treated  group,  however,  no  significant  in- 
crease in  malignancies  was  apparent  during  the  five 
years  of  the  study.  The  mechanism  responsible  for 
the  reduced  incidence  of  coronary  heart  disease  in  the 
Helsinki  study  is  difficult  to  define  since  patients  with 
variable  lipoprotein  patterns  participated  and  poten- 
tially beneficial  changes  in  several  of  the  lipoprotein 
fractions  were  observed.  However,  it  is  likely  that  the 
increase  in  HDL-cholesterol  played  a major  role  in 
reducing  the  incidence  of  cardiac  events. 

NEOMYCIN 

Neomycin  is  considered  a second  line  agent  for  the 
treatment  of  hypercholesterolemia  in  patients  unable 
to  tolerate  more  standard  therapy.^  It  is  a poorly  ab- 
sorbed antibiotic  that  lowers  LDL-cholesterol  levels 
by  inhibiting  the  intestinal  absorption  of  cholesterol. 
Typically  serum  LDL-cholesterol  levels  decrease  15% 
to  25%.  Like  other  aminoglycoside  antibiotics,  neo- 
mycin has  the  potential  to  cause  nephrotoxicity  and 
ototoxicity.  However,  these  complications  are  rela- 
tively uncommon  if  neomycin  is  not  prescribed  for 
patients  with  renal  impairment  or  those  with  gas- 
trointestinal diseases  that  might  allow  for  increased 
absorption  of  the  drug.^  More  commonly,  patients 
may  experience  abdominal  cramps  or  diarrhea.  The 
usual  dose  is  one  g twice  a day.  Hoeg  et  al  reported 
that  a regimen  of  neomycin  in  combination  with  nic- 
otinic acid  was  able  to  lower  LDL-cholesterol  levels 
by  45%  in  those  patients  able  to  tolerate  the  prescribed 
doses  of  both  drugs. 

DEXTROTHYROXINE 

Dextrothyroxine,  the  optical  isomer  of  1-thyroxine, 
can  lower  LDL-cholesterol  concentrations  by  10%  to  | 
20%.  The  drug  increases  LDL  catabolism  by  stimu- 
lating activity  of  hepatic  high  affinity  LDL-receptors. 
However,  the  hypocholesterolemic  effect  of  dextro- 
thyroxine is  achieved  at  the  expense  of  producing  a 
mild  state  of  thyrotoxicosis.^  Effective  doses  may  ex- 
acerbate angina,  and  cause  nervousness,  tremor, 
sweating,  and  cardiac  arrhythmias.  Bantle  et  al  dem- 
onstrated that  equivalent  doses  of  d-  and  1-thyroxine 


52  JOURNAL  VOL  140  MAY 


Fig.  Complementary  action  of  combined  therapy 
with  a bile  salt  sequestrant  plus  an  inhibitor 
of  HMG  CoA  reductase  in  the  treatment  of  hy- 
percholesterolemia (©  Nobel  Foundation, 
1986). 

(based  on  suppression  of  the  thyroid-stimulating  hor- 
mone response  to  thyrotropin  releasing  hormone) 
produced  comparable  decreases  in  LDL-cholesterol 
levels. D-thyroxine  is  usually  initiated  at  a dose  of 
2 mg  per  day.  The  dose  is  titrated  up  by  1 mg  incre- 
ments to  a maximal  dose  of  4 mg  to  6 mg  per  day. 
The  drug  should  not  be  used  in  patients  with  evidence 
of  cardiac  disease  or  older  individuals  who  might  have 
asymptomatic  coronary  stenoses.^'  ^ Due  to  its  effect 
on  accelerating  metabolism  and  its  potential  to  ex- 
acerbate coronary  heart  disease,  dextrothyroxine  has 
a very  limited  place  in  the  management  of  hypercho- 
lesterolemia. 

COMBINATION  THERAPY 

For  those  individuals  with  hypercholesterolemia  who 
do  not  achieve  a satisfactory  lowering  of  the  serum 
cholesterol  on  single  drug  therapy,  a combination  of 
drugs  may  enhance  the  therapeutic  response.  Patients 
who  are  heterozygotes  for  familial  hypercholester- 
olemia typically  need  treatment  with  more  than  a sin- 
gle agent  in  order  to  normalize  cholesterol  levels.  Pref- 
erably, agents  are  chosen  that  lower  cholesterol  levels 
by  different  mechanisms  of  action. ^ Bile  salt  seques- 
trants  together  with  nicotinic  acid  have  been  used 
successfully  for  many  years.  This  combination  is  par- 
ticularly helpful  to  lower  triglyceride  levels  in  patients 
who  develop  elevations  of  this  lipid  on  sequestrants 
alone.  When  used  together  total  cholesterol  levels  de- 
crease by  45%  and  LDL-cholesterol  by  55%. ® More 
recently,  the  addition  of  lovastatin  to  a bile  salt  se- 
questrant has  proved  extremely  successful  as  a hy- 
pocholesterolemic  regimen.  Lovastatin,  by  blocking 
the  enhanced  cholesterol  synthesis  that  occurs  when 


cholestyramine  or  colestipol  is  used  alone,  enhances 
the  increase  in  hepatic  LDL-receptors  and  augments 
the  therapeutic  response  (Fig).^  Typically,  a decrease 
of  55%  can  be  achieved  in  LDL-cholesterol  in  patients 
with  nonfamilial  hypercholesterolemia  and  hetero- 
zygotes for  familial  hypercholesterolemia.^^'  Many 
other  combinations  of  hypocholesterolemic  agents 
have  been  used  in  limited  numbers  of  patients.  Gen- 
eral recommendations  must  await  additional  studies 
evaluating  the  efficacy  and  side  effects  of  such  com- 
binations. ■ 

ACKNOWLEDGMENTS 

Thanks  to  Drs  Brown  and  Goldstein  and  the  Nobel 
Foundation  for  permission  to  reprint  the  figure. 

REFERENCES 

1.  Grundy  SM:  Cholesterol  and  coronary  heart  disease;  A new  era.  JAMA 
1986;256:2849-2858. 

2.  Lipid  Research  Clinics  Program.  The  lipid  research  clinics  coronary  pri- 
mary prevention  trial  results:  I Reduction  in  incidence  of  coronary  heart 
disease.  JAMA  1984;251:351-364. 

3.  The  Expert  Panel:  Report  of  the  National  Cholesterol  Education  Program 
expert  panel  on  detection,  evaluation,  and  treatment  of  high  blood  cho- 
lesterol in  adults.  Arch  Intern  Med  1988;148:36-69. 

4.  Frick  MH,  Elo  O,  Haapa  K,  et  al:  Helsinki  Heart  Study:  Primary-pre- 
vention trial  with  gemfibrozil  in  middle-age  men  with  dyslipidemia: 
Safety  of  treatment,  changes  in  risk  factors,  and  incidence  of  coronary 
heart  disease.  N Engl  J Med  1987;317:1237-1245. 

5.  Brown  WV,  Goldberg  IJ,  Ginsberg  HN:  Treatment  of  common  lipopro- 
tein disorders.  Prog  Cardiovasc  Dis  1984;27:1-20. 

6.  Illingworth  DR:  Lipid-lowering  drugs:  An  overview  of  indications  and 
optimum  therapeutic  use.  Drugs  1987;33:259-279. 

7.  Brown  MS,  Goldstein  JL:  A receptor-mediated  pathway  for  cholesterol 
homeostasis.  Science  1986;232:34-47. 

8.  Kane  JP,  Malloy  MJ,  Tun  P,  et  al:  Normalization  of  low-density-Upopro- 
tein  levels  in  heterozygous  familial  hypercholesterolemia  with  a com- 
bined drug  regimen.  N Engl  J Med  1981;304:251-258. 

9.  Lovastatin  Study  Group  II:  Therapeutic  response  to  lovastatin  (mevi- 
nolin)  in  nonfamilial  hypercholesterolemia:  A multicenter  study.  JAMA 
1986;256:2829-2834. 

10.  Havel  RJ,  Hunninghake  DB,  lUingworth  R,  et  al:  Lovastatin  (mevinolin) 
in  the  treatment  of  heterozygous  familial  hypercholesterolemia.  Ann  In- 
tern Med  1987;107:609-615. 

11.  Farnsworth  WH,  Hoeg  JM,  Brittain  EH,  et  al:  Testicular  function  in  type 
II  hyperlipoproteinemic  patients  treated  with  lovastatin  (mevinolin)  or 
neomycin.  J Clin  Endocrinol  Metab  1987;65:546-550. 

12.  Hoeg  JM,  Maher  MB,  Bou  E,  et  al:  Normalization  of  plasma  lipoprotein 
concentrations  in  patients  with  type  II  hyperlipoproteinemia  by  com- 
bined use  of  neomycin  and  niacin.  Circulation  1984;70:1004-1011. 

13.  Bantle  JP,  Hunninghake  DB,  Frantz  ID,  et  al;  Comparison  of  effectiveness 
of  thyrotropin-suppressive  doses  of  d-  and  1-thyroxine  in  treatment  of 
hypercholesterolemia.  Am  J Med  1984;77:475-481. 

14.  Vega  LG,  Grundy  SM:  Treatment  of  primary  moderate  h5^ercholester- 
olemia  with  lovastatin  (mevinolin)  and  colestipol.  JAMA  1987;257:33-38. 

15.  Illingworth  DR:  Mevinolin  plus  colestipol  in  therapy  for  severe  hetero- 
zygous famiHal  hypercholesterolemia.  Ann  Intern  Med  1984;101:598-604. 


Dr.  Levine  is  with  the  Dept  of  Medicine,  Section  of  Endocrinology,  at 

LSU  Medical  Center  in  Shreveport. 

Reprint  requests  should  be  sent  to  Steven  N.  Levine,  MD,  LSU  Medical 
Center,  Dept  of  Medicine,  Section  of  Endocrinology,  PO  Box  33932, 

Shreveport,  LA  71130. 


JOURNAL  VOL  140  MAY  55 


PROFFSSTOMAT  T TSTTNCS 

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TOURNAL 


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STA( 


Heart  transplantation:  The  Louisiana  experience 


ALSO:  MICROSURGERY  IN  BREAST  RECONSTRUCTION  SURGICAL  MANAGEMENT 

USING  THE  SUPERIOR  GLUTEUS  EOR  OE  IMPOTENCE: 

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JOURNAL 

J — 


""  OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY 

1988 

VOLUME  140  / NUMBER  6 / 

JUNE 

ARTICLES 

John  L.  Ochsner,  MD 

34 

Heart  transplantation: 

Clement  C.  Eiswirth  Jr,  MD 

The  Louisiana  experience 

Mary  Lyn  T.  Lu,  MD 

43 

Microsurgery  in  breast 

William  M.  Swartz,  MD 

reconstruction  using  the 
superior  gluteus  for  free 
tissue  transfer:  A case  report 

Neil  Baum,  MD 

47 

Surgical  management  of 
impotence:  New  modalities 

DEPARTMENTS 


2 

Information  for  Authors 

3 

ECG  of  the  Month 

7 

Otolaryngology/Head 

& Neck  Surgery  Report 

11 

Book  Reviews 

12 

Books  Received 

13 

Auxiliary  Report 

54 

Calendar 

59 

Classified  Advertising 

Cover  illustration  by  Barbara  Seide,  New  Orleans 


I 


INFORMATION  FOR  AUTHORS 


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Norton  W.  Voorhies,  MD,  Editor 


ECG  OF  THE  MONTH 


THE  COLD  FACTS 

JORGE  I.  MARTINEZ-LOPEZ,  MD 


The  12-lead  tracing  shown  left 
belongs  to  a 19-year-old  man. 
It  was  recorded  several  days 
after  a traumatic  fracture  of 
his  fifth  cervical  spine  with 
posterior  displacement.  Med- 
ications included  dexameth- 
asone  and  cimetidine. 


What  is  your  diagnosis? 
Elucidation  is  on  page  5. 


JOURNAL  VOL  140  JUNE  3 


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ECG  of  the  Month 

Case  presentation  is  on  page  3. 

DIAGNOSIS  — Spontaneous  hypothermia 

Profound  sinus  bradycardia  with  sinus  arrhythmia, 
at  rates  from  33  to  42  a minute,  is  present.  The  PR 
interval  is  normal.  QRS  complexes  appear  broad  and 
display  an  upward  notch  in  the  downstroke  of  the 
QRS  in  leads  1,2,3,  AVF,  and  V2  through  V6;  AVR 
shows  a notch  directed  downward.  Elevated  ST  seg- 
ments with  a concavity  downward  are  recorded  in 
leads  1,2,  AVR,  and  V2  through  V6.  Upright  T waves 
are  found  in  all  leads  except  AVR  and  display  a ter- 
minal notch  in  V3.  Lastly,  the  QT  interval  is  length- 
ened to  0.56  second. 

This  constellation  of  ECG  findings  is  consistent 
with  the  clinical  diagnosis  of  hypothermia  and  is  the 
subject  of  the  discussion  to  follow. 

DISCUSSION 

Hypothermia  — as  measured  with  a low-reading  rec- 
tal thermometer  — is  defined  as  central  body  tem- 
perature (core  body  temperature)  of  34°  C or  lower. 
This  condition  may  develop  as  a result  of  either  ac- 
cidental or  iatrogenic  exposure  to  low  environmental 
temperatures  and,  less  frequently,  it  is  secondary  to 
acute  medical  or  surgical  disorders  that  are  unrelated 
to  exposure  (spontaneous).  In  this  last  group,  hy- 
pothermia often  goes  unrecognized  because  conven- 
tional rectal  thermometers  do  not  record  temperatures 
lower  than  35°  C.  Hypothermia  may  occur  in  the  pres- 
ence or  absence  of  cardiac  disease. 

The  patient  whose  tracing  is  shown  here  was 
found  to  be  hypothermic  at  the  time  the  12-lead  ECG 
was  recorded.  However,  the  exact  core  body  tem- 
perature was  not  established  because  of  the  unavail- 
ability of  the  proper  type  of  rectal  thermometer.  The 
abnormal  ECG  findings  were  ascribed  to  hypother- 
mia. 

The  characteristic  ECG  features  found  in  hypoth- 
ermia are  predictable  and  reproducible  experimen- 
tally, appear  sequentially  as  body  temperature  drops 
below  normal,  and  disappear  gradually  with  rewarm- 
ing. Cold  core  body  temperatures  depress  cardiac  au- 
tomaticity.  Consequently,  the  majority  of  hypoth- 
ermic patients  show  sinus  rates  in  the  low  30s  to  the 


high  40s.  At  extremely  low  core  body  temperatures, 
some  patients  may  develop  atrial  fibrillation,  sino- 
ventricular  conduction  or  junctional  escape  rhythm. 

The  long  QT  interval  found  in  hypothermia  has 
been  attributed  to  increases  in  the  duration  of  ven- 
tricular repolarization  as  a result  of  myocardial  cooling 
and  not  to  delayed  ventricular  depolarization. 

One  of  the  most  important  clues  on  the  ECG  of 
the  hypothermic  patient  is  the  extra  deflection  or  notch 
recorded  at  the  QRS-ST  junction.  This  deflection, 
originally  described  by  Tomaszewski  in  1938,  has  been 
given  the  eponymic  designation  of  the  Osborn  wave. 
Other  terms  applied  to  this  deflection  include:  J de- 
flection, J wave,  camel  hump  wave,  dromedary  wave, 
and  hypothermic  hump.  The  emergence  of  the  Os- 
born wave  on  the  ECG  is  inversely  related  to  the  core 
body  temperature,  but  its  mechanism  of  production 
remains  unclear.  This  wave  may  be  overlooked  if  only 
a single  ECG  lead  is  recorded  or  examined.  The  Os- 
born wave  is  most  commonly  found  in  limb  leads  2,3, 
AVF,  and  precordial  leads  V5  and  V6,  and  is  directed 
upward;  when  present  in  AVR  and  VI,  it  is  directed 
downward.  As  hypothermia  deepens,  the  Osborn 
wave  tends  to  appear  in  all  leads  and  become  more 
anteriorly  oriented  in  the  precordial  leads.  Although 
the  amplitude  and  duration  of  the  Osborn  wave  di- 
minish gradually  with  rewarming,  in  very  few  cases 
it  may  persist  for  some  time  thereafter  or  perma- 
nently. 

As  an  isolated  ECG  finding,  the  Osborn  wave  is 
not  diagnostic  of  hypothermia.  This  wave  has  been 
seen  frequently  in  normothermic  young  adults  who 
have  no  demonstrable  cardiac  or  extracardiac  disease. 

In  patients  with  induced  and  accidental  hypo- 
thermia, fine  oscillations  of  the  baseline  due  to  muscle 
tremor  artifacts  are  recorded  often.  These  artifacts 
make  it  difficult  to  identify  atrial  electrical  activity  and 
to  determine  the  cardiac  rhythm.  In  such  cases,  di- 
agnostic procedures  that  may  be  considered  include 
echocardiography  and  His  bundle  electrography.  M- 
mode  echocardiography  is  helpful  in  identifying  "A" 
waves.  In  some  patients,  however,  "A”  waves  were 
recorded  even  though  P waves  were  absent  from  the 
ECG.  Although  His  bundle  electrography  may  be  of 
diagnostic  utility,  it  is  prudent  not  to  use  this  invasive 
procedure  because  hypothermic  patients  are  already 
critically  Ul  and  experience  a high  mortality  rate. 

The  electrical  causes  of  death  in  hypothermic  ► 


JOURNAL  VOL  140  JUNE  5 


patients  include  ventricular  fibrillation  and  cardiac 
asystole.  Most  often,  the  terminal  rhythm  is  cardiac 
asystole. 

There  you  have  it.  Those  are  . . . the  cold  facts! 


SELECTED  REFERENCES 

1.  Drake  CE,  Flowers  NC:  ECG  changes  in  hypothermia  from  sepsis  and 
unrelated  to  exposure.  Chest  1980;77:685-686. 

2.  Okada  M,  Nishimura  F,  Yoshino  H,  et  al:  The  J wave  in  accidental  hy- 
pothermia. / Electrocardiol  1983;16:23-28. 

3.  del  Bosco  CG,  Poderoso  JJ,  BiancoUni  CA,  et  al:  Hallazgos  electrocardi- 
ograficos  en  la  hipotermia  secondaria  a enfermedades  agudas.  Medicim 
1983;43:629-638. 


4.  Rankin  AC:  Cardiac  arrhythmias  during  rewarming  of  pahents  with  ac- 
cidental hypothermia.  Brit  Med  J 1984;289:874-877. 

5.  Okada  M:  The  cardiac  rhythm  in  accidental  hypothermia.  J Electrocardiol 
1984;17:123-128. 


Dr.  Martinez-Lopez  is  a specialist  in  cardiovascular  diseases  affiliated 
with  the  Cardiology  Service,  Dept  of  Medicine  at  William  Beaumont 
Army  Medical  Center  in  El  Paso,  Texas. 

The  opinions  and  assertions  contained  herein  are  the  private  views  of  the 
author  and  not  to  be  construed  as  official  or  as  reflecting  the  views  of 
the  Dept  of  the  Army  or  Dept  of  Defense. 

Reprints  will  not  be  available. 


“The  Louisiana  Geriatric 
Assessment  Center  helps  me 
keep  my  independence.” 


“When  Robert  passed  away,  I went  through  a time  of 
radical  adjustment  and  some  illness. 

“My  doctor  was  great!  And  when  he  saw  that  my 
non-medical  needs  extended  from  financial  counseling 
to  a grocery  delivery  service,  he  suggested  I visit  the 
Louisiana  Geriatric  Assessment  Center. 

“There,  through  a program  called  Care  Management, 
Assessment  Center  specialists  carefully  studied  my  living 
situation  and  helped  me  find  the  services  1 needed  to 
keep  my  independence. 

“They  worked  carefully  within  my  limited  budget. 

Most  importantly,  they  kept  in  close  touch  until  1 was  up 
and  on  my  feet  again. 

“Today  Fm  happy  and  healthy.  And  Fm  tremendously 
grateful  to  my  doctor  and  Care  Management.” 


□ Yes,  1 would  like  more  information  on  Care  Manage- 
ment and  the  Louisiana  Geriatric  Assessment  Center. 

□ 1 can  provide  a service  helpful  to  older  adults  and 
would  like  to  be  included  in  the  Care  Management 
Service  Index. 

Name:  


Phone  #: 

Mail  Coupon  to; 

The  Louisiana  Geriatric  Assessment  Center 

3888  North  Boulevard,  Baton  Rouge,  Louisiana  70806 


City/State: 


6 JOURNAL  VOL  140  JUNE 


OTOLARYNGOLOGY/ 

HEAD  & NECK  SURGERY  REPORT 


CHRONIC  HALITOSIS  FROM 
TONSILLOLITHS: 


A COMMON 


STEVEN  M.  FLETCHER,  MD; 


Chronic  halitosis  from  tonsilloliths  represents  a 
common^  yet  oftentimes  overlooked  problem  in 
clinical  otolaryngologic  practice.  A case  of  a 28- 
year-old  woman  with  this  condition  is  presented 
followed  by  a discussion  of  its  pathophysiology 
and  management.  The  most  common  etiologies  of 
chronic  halitosis  are  also  indicated. 


ETIOLOGY 


PAUL  A.  BLAIR,  MD,  FACS 


A28-year-old  woman  gave  a history  of  chronic  in- 
termittent halitosis  which  had  been  present  for 
several  years  and  which  had  remained  unresponsive 
to  long-term  use  of  various  mouth  washes  and  per- 
oxide rinses.  As  a child,  she  had  suffered  from  mul- 
tiple episodes  of  follicular  tonsillitis  which  had  re- 
solved following  medical  therapy.  On  rare  occasions 
in  her  adult  life,  she  had  continued  to  have  bouts, 
the  most  recent  of  which  having  occurred  several 
months  previously.  She  denied  any  history  of  upper 
respiratory  tract  infections,  nasal  or  paranasal  sinus 
disorders,  smoking,  dental  or  oral  cavity  disease,  and 
other  known  medical  conditions.  Family  history 
showed  her  mother  had  also  suffered  from  chronic 
halitosis  for  which  she  was  treated  by  a tonsillectomy 
for  cryptic  follicular  tonsillitis  with  tonsilloliths  with 
complete  resolution  of  her  problem.  Physical  exami- 
nation of  the  patient  on  admission  was  remarkable 
only  for  moderately  enlarged  cryptic  tonsils  with  nu- 
merous small  caseous  plugs  and  multiple  calcareous 
particles  protruding  from  the  crypts  of  the  tonsils.  No 
other  demonstrable  lesions  of  the  upper  aerodigestive 

JOURNAL  VOL  140  JUNE  7 


tract  were  noted;  adequate  dental  hygiene  was  ap- 
parent. She  subsequently  underwent  an  elective  ton- 
sillectomy with  an  unremarkable  postoperative  re- 
covery. The  halitosis  condition  has  been  under 
complete  control  under  a follow-up  period  of  one  year. 

Chronic  halitosis  is  a distinctly  unpleasant  odor 
to  the  breath.  Etiology  is  due  primarily  to  five  groups 
of  conditions.  Septic  or  putrefactive  disease  within 
the  oral  cavity,  nose,  or  paranasal  sinuses  is  the  group 
most  often  causing  halitosis.  Chronic  tonsillitis  with 
tonsilloliths  constitutes  one  of  the  more  common 
members  of  this  group.  Stomatitis,  gingivitis,  glos- 
sitis, periodontal  disease,  and  carious  teeth  with  en- 
trapped fermenting  food  particles  all  reflect  local  de- 
composition of  the  mouth  from  which  the  fetid  odor 
is  generated.  Nasal,  pharyngeal,  and  sinus  infectious 
conditions  (ie,  suppurative  rhinosinusitis,  syphilis, 
carcinoma  of  the  upper  aerodigestive  tract,  foreign 
bodies  [in  children],  chondronecrosis  or  osteonecrosis 
of  the  nasal  skeleton,  allergic  catarrh,  atrophic  rhinitis 
and  chronic  pharyngitis)  can  all  give  rise  to  foulness 
of  the  breath. 

Perhaps  the  second  most  common  etiology  of  hal- 
itosis would  be  such  ingested  or  inhaled  substances 
as  onions,  garlic,  paraldehyde,  tobacco  smoke,  alco- 
hol, and  certain  drugs  whose  volatile  products  are 
excreted  at  least  in  part  by  the  lungs  or  salivary  glands. 

Putrefactive  diseases  of  the  lung  may  cause  fetid 
breath  odor.  The  underlying  thoracic  pathology  is 
generally  indicated  by  abundant  putrid  sputum,  fre- 
quent chest  symptoms,  and  usually  readily  apparent 
abnormal  thoracic  physical  signs.  Pyogenic,  tuber- 
culous, or  other  granulomatous  diseases  of  the  lung 
presenting  as  bronchitis,  gangrene,  bronchiectasis, 
empyema,  or  abscess  may  generate  malodorous 
breath.^ 

Severe  alimentary  tract  or  peritoneal  disorders 
may  uncommonly  cause  halitosis.  Foul  breath  usually 
does  not  signify  gastrointestinal  disorders  because  the 
esophagus  is  normally  collapsed  and  anatomically 
separate  from  the  airway.  Certain  disease  states  such 
as  tracheoesophageal  fistula,  bronchoesophageal  fis- 
tula,^ or  gastrointestinal  disturbances  associated  with 
severe  gastroesophageal  reflux  may  precipitate  a com- 
munication between  the  esophagus  and  the  upper 
respiratory  tract.  A disagreeable  taste  and  odor  may 
emanate  from  this  communication.  Some  systemic 
diseases  have  characteristic  odors:  diabetic  ketoaci- 


dosis a fruity  odor,  hepatic  failure  a musty  or  fishy 
odor,  and  azotemia  a uriniferous  odor. 

Psychogenic  causes  namely  the  rumination  syn- 
drome or  merycism  and  hypochondriacal  states  can 
contribute  to  halitosis.  Obsession  with  one's  self- 
cleanliness and  paranoid  delusions  of  self-destruction 
of  one's  body  organs  have  both  been  delineated  as 
the  underlying  disorder  in  many  psychiatric  patients 
with  halitosis. 

Tonsilloliths  are  spiculated  concretions  of  calcar- 
eous or  gritty  particles  which  occur  as  a result  of  dep- 
osition of  inorganic  salts  in  the  debris  that  accumu- 
lates within  the  crypts  of  tonsils  in  chronic  follicular 
tonsillitis.  These  calculi,  which  occur  much  more  fre- 
quently in  adults  than  in  children,  are  usually  rounded 
or  oval  particulate  matter.  They  may  vary  in  size  from 
multiple  small  stones  within  the  substance  of  the  ton- 
sil or  tonsillar  crypts  to  a single  large  stone  which  may 
be  partially  or  completely  embedded  in  the  tonsil.^ 
Tonsilloliths  represent  the  product  of  repeated  in- 
flammatory episodes  of  the  tonsils  which  often  re- 
main clinically  subacute.  The  cryptic  openings  on  the 
exterior  of  the  tonsil  often  develop  fibrosis  with  en- 
trapment of  squamous  debris,  particulate  food  matter, 
and  normal  oral  flora  including  bacterial,  fungal,  and 
actinomyces-like  organisms.  The  fermentation  proc- 
ess within  this  inflamed  tonsillar  pocket  then  gener- 
ates the  putrid  odor  and  hence  clinical  halitosis. 

Calculi  of  the  tonsil  must  be  differentiated  from  1 
other  clinical  entities,  namely:  calcified  granulomas,  ! 
foreign  bodies  (especially  in  children),  malignant  neo- 
plasia of  the  tonsillar  region,  embryonic  branchial  arch 
osseous  or  cartilaginous  rests,  or  an  elongated  styloid 
process  protruding  from  the  posterior  aspect  of  the 
tonsillar  fossa. ^ 

Clinically  most  patients  present  as,  in  the  case 
report,  with  a history  of  multiple  episodes  of  recurrent 
acute  tonsillitis  in  childhood  and  subsequently  as 
adults  may  complain  of  foreign  body  sensation,  bad 
taste  in  the  mouth,  nonspecific  odynophagia,  chronic  ^ 
cough  or  gagging,  or  otalgia. 

Physical  examination  usually  reveals  bilateral 
cryptic  tonsils  which  often  contain  caseous  plugs  of 
debris  or  tonsilloliths  with  or  without  local  inflam-  j 
mation.  A careful  search  for  the  multiple  other  causes  | 
of  halitosis  especially  of  the  oral,  nasal,  and  sinus  i 
cavities  is  indicated  to  eliminate  those  conditions.  Ex-  ! 
elusion  of  periodontal  or  apical  tooth  infections  or 
food  particle  impactions,  even  in  persons  exercising 


8 JOURNAL  VOL  140  JUNE 


regular  tooth  brushing  and  oral  hygiene,  is  essential 
in  establishing  the  cryptic  tonsil  as  the  culprit. 

The  treatment  of  tonsilloliths  and  their  associated 
chronic  tonsillitis,  which  may  be  subclinical,  is  re- 
moval of  the  tonsillar  calculi  when  possible,  as  with 
a single  stone  or  a limited  number  of  larger  stones  or 
tonsilloliths.  Temporizing  measures  of  frequent  mouth 
rinses  or  peroxide  gargles  following  all  meals  and 
snacks  can  achieve  sufficient  control  of  halitosis  in 
some  patients  but  requires  habitual  long  term  daily 
usage.  The  definitive  removal  of  the  nidus  of  this 
condition,  by  tonsillectomy,  remains  the  most  satis- 
factory permanent  solution  to  this  problem. 

In  summary,  tonsilloliths  with  their  associated 
! chronic  follicular  tonsillitis  represent  one  of  the  more 
common,  yet  oftentimes  overlooked,  causes  of  chronic 
halitosis  in  adults.  The  various  common  etiologies  of 
, halitosis  are  presented  with  control  of  the  condition 
' obviously  resting  upon  control  of  the  underlying  dis- 
1 ease  process.  Following  elimination  of  other  common 
4 causes  of  halitosis,  especially  those  arising  from  the 
I oral  cavity,  low-grade,  often  subclinical,  cryptic  ton- 
i sillitis  with  calculi  and  caseous  debris  should  be  con- 
1 sidered  as  the  cause  of  malodorous  breath.  When  es- 
tablished as  the  underlying  cause  of  halitosis, 
tonsilloliths  may  be  definitively  treated  to  achieve 
( lasting  resolution.  ■ 


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REFERENCES 

1.  Hart  FO:  French's  Index  of  Differential  Diagnosis,  ed  12.  Bristol,  England,  J 
Wright  & Sons  Ltd,  1985. 

2.  Lawson  RAM,  Carroll  K:  Delayed  halitosis  — A rare  cause.  Postgrad  Med 
} 1982;58(675);52-54. 

3.  Ballenger  JJ:  Diseases  of  the  Nose,  Throat,  Ear,  Head  and  Neck,  ed  13.  Phil- 
adelphia, Lea  and  Febiger,  1969. 

4.  Paparella  MM,  Shumrick  DA:  Otolaryngology,  ed  2,  vol  III.  Philadelphia, 
WB  Saunders  Co,  1980. 


Dr  Fletcher  is  a resident  in  the  Dept  of  Otolaryngology-Head  Neck 
Surgery  at  Tulane  Medical  School  in  New  Orleans. 

Dr  Blair  is  professor  of  Otolaryngology-Head  Neck  Surgery  at  Tulane 

Medical  School  in  New  Orleans. 


JOURNAL  VOL  140  JUNE  9 


The  Advantages  Of  Magnetic  Resonance  Imaging  Are  Gearly  Seen. 


The  clarity  of  MRI  is  just  part  of  what 
can  be  quickly  seen. 

Now  your  patients  can  be  quickly 
seen  for  diagnostic  MR  imaging  as  a re- 
sult of  East  Jefferson  General  Hospital’s 
permanent  1.5  Tesla  circular  polarized 
magnet  in  our  new,  permanent  Magnetic 
Resonance  Imaging  Center.  Because, 
along  with  the  most  up-to-date  MRI 
technology  and  our  staff  of  medical  and 
technical  speciahsts,  the  center  utilizes 


a scheduling  and  report  turn-around 
system  to  make  this  extraordinary  serv- 
ice convenient  for  you  and  your  patients. 

MRI  has  proven  itself.  Its  combi- 
nation of  magnetic  fields,  radio  sound 
waves  and  powerful  computer  creates 
detailed  images  of  many  tissue  areas  we 
couldn’t  see  as  clearly  before-particu- 
larly  in  the  cranial  and  spinal  areas. 

Our  experience  with  MRI  goes 
beyond  East  Jefferson  General’s  new 


permanent  center  for  it.  We  are  the 
hospital  that  introduced  this  diagnostic 
breakthrough  to  the  region.  And  our 
periodical  publication,  “MRI  Update,” 
furnishes  up-to-date  information  on  this 
complicated  new  specialty. 

So  call  us  at  456-5154  for  a per- 
sonal tour  of  our  facility,  or  to  consult 
about  the  possible  applications  of  MRI 
for  your  patients.  You’ll  see  all  its  advan- 
t^es.  Clearly. 


Magnetic  Resonance  Imaging  Center 

East  Jefferson  General  Hospital 

Higher  Standards.  Outstanding  Doctors. 


I 


PHOTOGRAPHY  COURTESY  OF  SIEMENS  MEDICAL  SYSTEMS,  INC. 


Frank  J.  Ilardi,  MD,  Editor 


BOOK  REVIEW 


PRIMARY  CARE  OF  CANCER:  Recommendations 
for  Screening,  Diagnosis  and  Management 
Edward  A.  Mortimer  (ed):  Case  Western  Reserve 
School  of  Medicine,  Cleveland,  1987,  195  pages. 

by  MICHAEL  R.  MOORE  SR,  MD,  FACE 


PRIMARY  Care  of  Cancer,  called  the  “Plum  Book," 
is  a diminutive  volume  when  compared  with  its 
company  on  the  shelf  of  oncology  reference  texts.  This 
paperback  book  was  written  by  31  authors,  mostly 
physician  specialists  and  subspecialists,  from  Case 
Western  Reserve  University  and  the  Cleveland  Clinic. 
The  book  provides  concise  and  practical  information 
and  is  designed  as  a quick  and  ready  reference  for 
the  primary  care  physician  encountering  oncology  pa- 
tients. 

The  29  chapters  cover  the  30  most  common  le- 
sions reported  to  the  cancer  registry  in  the  Cleveland 
region,  and  thus  reflects  frequently  encountered  can- 
cers seen  in  community  hematology/oncology  prac- 
tices. Each  chapter  is  divided  into  the  following  sec- 
tions: description  (containing  the  standard  staging  by 
the  American  Joint  Committee  on  Cancer  schema,  the 
International  Tumor,  Nodal,  Metastasis  system,  or  a 
disease-specific  staging  system),  epidemiology  and  risk 
factors,  etiology,  prevention,  screening,  signs  and 
symptoms,  diagnostic  tests,  treatment  and  prognosis, 
and  post-treatment  follow-up.  The  final  chapter  cov- 
ers home  care  for  the  terminally  iU. 

The  book  is  straightforward,  pragmatic,  and  only 
occasionally  overly  abridged.  The  Plum  Book  is  a syn- 
opsis, but  does  not  read  like  a Reader's  Digest  con- 
densed book  that  only  skims  the  high  points.  The 
sections  on  epidemiology,  risk  factors,  and  preven- 
tion are  well  covered.  The  treatment  sections  are  less 
detailed  and  do  not  address  the  controversies  fre- 
quently encountered  in  oncology.  In  my  opinion, 
many  treatment  recommendations  are  overly  con- 
servative and  fail  to  reflect  the  move  to  earlier  and 


more  aggressive  (frequently  multimodality)  therapy 
being  developed.  In  defense,  however,  the  introduc- 
tion states  that  “cancer  therapy  in  the  1980s  is  suffi- 
ciently complex  that  sophisticated  subspecialty  care 
is  usually  indicated."  The  book  consistently  reflects 
that  philosophy  and  avoids  specific  and  detailed  treat- 
ment recommendations. 

I think  it  would  have  been  helpful  if  a short  bib- 
liography or  reading  list  had  followed  each  chapter. 
Also,  a section  describing  the  basics  of  cell  growth, 
oncogenesis,  radiation  therapy,  and  cancer  chemo- 
therapy would  provide  a common  framework  for  the 
discussions  which  followed. 

This  small  volume,  though  written  for  the  pri- 
mary care  physician,  is  packed  with  enough  clinically 
useful  material  to  catch  the  interest  of  the  hematol- 
ogist/oncologist and  holds  its  own  even  against  the 
definitive  tomes  on  the  subject.  The  Plum  Book  de- 
serves its  place  on  the  shelf  of  any  physician  respon- 
sible for  patients  with  malignancy.  ■ 


Dr  Moore  is  a hematologist/oncologist  at  Willis-Knighton  Medical 
Center  and  a clinical  assistant  professor  of  medicine  at 
LSU  School  of  Medicine  in  Shreveport. 

Requests  for  reprints  should  be  sent  to  Dr  Moore,  PO  Box  3991, 

Shreveport,  LA  71133. 


JOURNAL  VOL  140  JUNE  11 


Successful  Procedures  for 
Male  & Female  Infertilify 


• In  Vitro  Fertilization/  • Endometriosis  Medical  & 
Embryo  Transfer  Surgical  Management 

• Gamete  Intrafallopian  • Complete  Andrology 

Transfer  G.I.F.T.  (Male)  Laboratory 

• Micro  Laser  Surgery  • Ovulation  Induction 

• Reversal  of  Tubal  • Hormone  Analysis 

Ligation  • Embryo  Preservation 

WILLIAM  E.  RONIGER.  M.D.  HEBER  E.  DUNAWAY,  JR.,  M.D. 

Board  Certified,  American  College  Board  Certified,  Board  Eligible, 

of  Obstetrics  and  Gynecology  American  College  American  Board  of 

of  Obstetrics  Reproductive 

and  Gynecology  Endocrinology 

FERTIUTY  CENTER 

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BOOKS  RECEIVED: 

The  JOURNAL  seeks  reviews  of  the  following  books.  Interested 
physicians  should  contact  Frank  f.  Ilardi,  MD,  Book  Review  Editor, 
5000  Highway  190,  Suite  D-3,  Covington,  LA  70433. 

PRACTICAL  MICROSCOPIC  HEMATOLOGY: 

A MANUAL  FOR  THE  CLINICAL  LABORATORY 
AND  CLINICAL  PRACTICE 

Fritz  Heckner,  MD,  H.  Peter  Lehmann,  PhD,  Yuan  S.  Kao, 
MD;  Baltimore,  Urban  & Schwarzenberg  Inc,  1988,  97  pages. 

CLINICAL  ELECTROCARDIOGRAPHY: 

A PRIMARY  CARE  APPROACH 

Ken  Grauer,  MD,  R.  Whitney  Curry,  Jr,  MD;  Oradell,  N], 
Medical  Economics  Books,  1987,  544  pages. 

OB/GYN  EMERGENCIES:  THE  FIRST  SIXTY  MINUTES 
Roy  Farrell,  MD  (ed);  Rockville,  MD,  Aspen  Publishers  Inc, 

1986,  340  pages. 

ENDOCERVICAL  CARCINOMA: 

A CERVICOSCOPIC  ATLAS 

Minoru  Ueki,  MD;  St  Louis,  Ishiyaku  Euroamerica  Inc,  1987, 
90  pages. 

THE  CLINICAL  GENETICS  HANDBOOK 

Ruth  Berini  (ed);  Oradell,  NJ,  Medical  Economics  Books,  1986, 
385  pages. 

INTERPRETING  CARDIAC  DYSRHYTHMIAS 

Marcus  Wharton,  MD,  Nora  Goldschlager,  MD;  Oradell,  NJ, 
Medical  Economics  Books,  1986,  241  pages. 

NEUROLOGY:  PROBLEMS  IN  PRIMARY  CARE 

James  L.  Bernat,  MD,  Frederick  M.  Vincent,  MD;  Oradell, 

NJ,  Medical  Economics  Books,  1987,  656  pages. 

INFORMED  CONSENT:  A SURVIVAL  GUIDE 

Donald  J.  Palmisano,  MD,  JD,  Hebert  J.  Mang  Jr,  JD;  New 

Orleans,  Invictus  Publishing  Co,  1987,  47  pages. 

TO  BE  OR  NOT  TO  BE  HUMAN: 

THE  TFIAITS  OF  HUMAN  NATURE 

Ben  Freedman,  MD;  New  York,  Vantage  Press,  1987,  509 

pages. 

THE  AGE  OF  MIRACLES 

Guy  Williams;  Chicago,  Academy  Chicago  Publishers,  1987, 
221  pages. 

PRIMARY  CARE  OF  CANCER 

Edward  A.  Mortimer  Jr,  MD  (ed);  Cleveland,  Case  Western 
Reserve  University  School  of  Medicine,  1987,  190  pages. 

HEALING  INTO  LIFE  AND  DEATH 

Stephen  Levine;  Garden  City,  NY,  Anchor  Press/Doubleday, 

1987,  290  pages. 

SICKLE-CELL  ANEMIA  AND  THALASSEMIA 

Newfoundland,  Canada,  Canadian  Sickle-Cell  Society,  1987. 


12  JOURNAL  VOL  140  JUNE 


Jackie  Tucker,  LSMSA  President 


AUXILIARY  REPORT 


PHYSICIANS’  HEALTH: 

THE  AUXILIARY’S  ROLE 

ELLOUISE  B.  SNEED 


SEVERAL  YEARS  AGO, 
the  American  Med- 
ical Association  (AMA) 
and  the  American  Med- 
ical Association  Auxil- 
iary (AMAA)  recog- 
nized the  need  to  assist 
physicians  and  their 
spouses  to  maintain  or 
regain  the  same  health 
status  promoted  for 
their  patients.  With 
increasing  numbers  of 
impairment,  physical 
illnesses,  litigation 
actions,  physicians  leaving  practice  at  an  earlier  age, 
and  physician  suicide  rates,  the  AMA  and  AMAA 
implemented  programs  to  educate  physicians  and  their 
families  of  available  support  resources.  Programs  were 
begun  to  present  potentially  unhealthy  factors  af- 
fecting physicians  and  their  families.  It  was  the  AMA's 
goal  to  relay  this  information  with  viable  answers  or 
solutions. 


The  Louisiana  State  Medical  Society  (LSMS)  be- 
gan its  first  steps  toward  an  impairment  program  in 
1981.  When  the  Impaired  Physicians  Committee  of 
the  LSMS  was  granted  full  committee  status  in  1984, 
the  Auxiliary  was  given  the  mission  of  educating  phy- 
sician spouses  about  its  existence  and  purpose.  Opal 
P.  McBride  (wife  of  WMam  A.  McBride,  MD)  was 
instrumental  in  birthing  this  effort.  Mrs  McBride's 
work  on  the  Impaired  Physicians  Committee  was 
greatly  influenced  by  the  groimdwork  laid  by  the  1975- 
76  LSMSA  President,  Dee  Cloyd  (wife  of  William  P. 
Cloyd  Jr,  MD).  Mrs  Cloyd  had  been  the  first  to  ap- 
point a Committee  within  the  Auxiliary  to  promote 
the  health  of  our  physicians  in  Louisiana. 

The  year  1988  finds  the  Auxiliary  assisting  in  a 
much  broader  role.  The  challenge  is  to  educate.  The  idea 
is  to  educate  physician  spouses  that  the  best  support 
system  is  another  physician  spouse.  Within  the 
framework  of  the  Auxiliary,  individual  or  collective 
support  can  be  given  to  those  families  experiencing 
a severe  physical  illness,  mental  illness,  early  or  reg- 
ular retirement,  a litigation  process,  or  death.  The 
Auxiliary  can  assist  spouses,  other  physicians,  the  ► 

JOURNAL  VOL  140  JUNE  13 


LSMS  by  being  a discriminate  listener,  by  avoiding 
gossip,  and  by  being  an  ear  to  the  pulse  of  the  com- 
munity's feelings. 

The  LSMS  is  encouraging  each  local  auxiliary  to 
promote  wellness  for  their  members  and  spouses,  and 
to  offer  assistance  to  the  local  medical  society  in  im- 
plementing the  LSMS  Impaired  Physicians  Program, 
Each  auxiliary  can  begin  with  awareness,  followed  by 
education,  genuine  concern,  and  encouragement  for 
those  families  experiencing  distress.  From  these  of- 
fered challenges,  rooted  in  the  history  of  prior  lead- 
ership, will  grow  a strong  health  care  support  for  the 
medical  family.  ■ 


Mrs  Sneed  (wife  of  Gary  A.  Sneed,  MD)  is  chairman  of  the 
Physicians  Health  Committee  of  the  LSMS  Auxiliary. 


NAVY  MEDICINE 

BOARD-CERTIFIED  PHYSICIANS 
SENIOR  RESIDENTS 

The  Navy  is  currently  offering  employment 
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Come  join  our  team  of  professionals.  Let's  discuss 
your  future  in  medicine.  Varied  locations  available 
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Call:  (504)  948-5542  (collect  if  necessary) 

BE  THE  DOCTOR  YOU  WANT  TO  BE. 

IN  THE  NAVY 


14  JOURNAL  VOL  140  JUNE 


Outgoing  President 
james  W.  Vildibill  Jr, 
MD  (left)  passes  the 
gavel  and  presidency 
to  1 988-89  President 
Daniel  H.  Johnson  Jr, 
MD  at  the  closing 
session  of  House  of 
Delegates. 


T 


he  1988  House  of  Delegates 
convened  at  the  108th  Annual  Meeting 
of  the  Louisiana  State  Medical  Society  on  March  11-13 
at  the  Civic  Center  in  Lake  Charles,  Louisiana. 


JOURNAL  VOL  140  JUNE  21 


EVENTS  OF 


Hotchkiss,  MD  spoke  at  the 
Delegates  Luncheon  and  ad- 
dressed some  of  the  major 
issues  facing  medicine  in- 
cluding professional  liability, 
Medicare,  peer  review,  and 
the  AMA's  ^Congressional 


LAMPAC 
Fourth’'*® 
District 
Alternate 
Director 
it' 'Robert 
Haley,  MD 
makes^a  s; 
presentation 
the  parish  ^ 
medical 
societies 
participating 
■a”””-,' 

iM&M 


alienge. 


B Outgoing  Auxiliary 
r President  Sancy 
; McCool  is  congrat- 
ulated by  James  W. 
Vildibill  Jr,  MD  at  the 
President's  Dinner 


LAMPAC  Chairman 
Howard  A.  Nelson, 
MD  outlined  the 
tremendous  success  in 
electing  a significant 
number  of  LSMS  sup- 
ported candidates  in 
the  recent  statewide 
elections. 


22  JOURNAL  VOL  140  JUNE 


THE  108th  ANNUAL  MEETING 


i 


1 


* 


Slit 


rJ;.  ' 


.-f 


■i-  '.'  * • 


At  the  MecScxrfegd  Pand 
Discussion,  David  Drez, 
MD  (center)  talks  about 
a hypothetical  case  iiv 
vtdving  attorneys  and 
physicians.  Among  the 
oth€»'  partic^^atnts  wt^re 
the  Honorable  Arthur  ]. 
Ptanchard  (left)  and  at- 
torney' Robert  Thomas 
(right). 


was  congratulated  for  T7 
year$  of  distinguished  ser- 
vice as  JOURNAL  editor 

K%/  C nna/Xkt  C MFl 


JOURNAL  VOL  140  JUNE  23 


ADDRESS  OF  THE 

PRESIDENT 


//. 


Our 

cohesiveness  will 
improve  our 
effectiveness  in 
helping  to  shape 

social  changes  that  can  provide  the 
people  we  serve  with  a 
better  quality  of  life. 

JAMES  W.  VILDIBILL  JR,  MD 


The  past  year  has  definitely  been  an 
interesting  one  for  me.  1 have 
enjoyed  the  privilege  of  serving  as  your 
president.  The  position  has  led  me 
down  a road  that  personally  has  been 
very  exciting  and  rewarding.  In  this 
journey  over  the  past  year,  I have  seen 
and  observed  many  events  that  are  af- 
fecting our  lives  and  our  profession.  Let 
me  take  just  a few  moments  this  mor- 
ning to  share  some  of  my  observations. 

We  are  positively  in  the  high-tech 
age  of  medicine.  There  will  no  doubt 
continue  to  be 
an  increase  in 
the  number 
and  complexity 
of  real  advances 
in  medical 
technology.  For 
example,  ad- 
vantages to 
physicians,  and 
especially  our 
patients,  are  ob- 
vious in  our 
present  ability 
to  eliminate 
many  urinary 
stones  with  ex- 
tracorporea  I 
shock  wave 
lithotripsy.  This 
high-technol- 
ogy approach  is 
so  much  more 
//  satisfying  than 

traditional  "cut- 
ting for  the 

stone."  Another 
example  of  our 
progress  Is  intraluminal  coronary 

angioplasty  that  often  can  accomplish 
the  same  result  as  a coronary  artery 
bypass.  Few,  perhaps  none  of  us, 
would  choose  a split  sternum  or  a flank 
incision  if  there  were  an  alter- 

native ...  and  now  there  is. 

Lots  more  is  coming,  such  as  im- 
plantable insulin  pumps  that  measure 
out  insulin  in  response  to  changing 
blood  sugar  levels.  Self-contained  con- 
tinuous monitoring  of  blood  sugar 
levels  is  an  integral  part  of  this  pump. 
This  example  is  not  typical  of  the 


mega-buck,  hospital-based  equipment 
we  so  frequently  cite  as  examples  of 
state-of-the-art  medicine. 

The  allure  of  these  new  and  expen- 
sive tools  of  medicine  is  causing  a shor- 
tage of  physicians  in  small  com- 
munities. Increasingly,  our  hospitals 
are  the  only  ones  who  can  afford  many 
of  these  advances.  In  many  instances, 
this  has  changed  practice  patterns, 
often  in  favor  of  hospital-based  physi- 
cians. This  trend  could  precipitate  fric- 
tion among  physicians  unless  we  all 
think  and  act  like  physicians  first,  and 
specialists  second.  We  need  to  fight  the 
source  of  our  problem,  not  ourselves. 

GOVERNMENT'S  JOB  IS  TO  GOVERN,  and  it 
is  certainly  exercising  its  prerogative 
when  it  comes  to  medicine.  Our  very 
success  in  providing  quality  health  care 
for  the  formerly  untreatable,  as  well  as 
better  health  care  for  all,  has  con- 
tributed significantly  to  the  rising  costs 
of  medical  care.  Government's  efforts 
to  control  these  costs  has  resulted  in  a 
plethora  of  conflicting  rules  and 
regulations. 

Professional  review  organizations, 
set  up  to  control  Medicare  costs,  are 
now  trying  to  justify  their  existence  by 
controlling  quality.  We  physicians 
have  serious  concerns  that  the  PRO 
(Peer  Review  Organization) 
"cookbook"  approach  to  medicine  is 
having  a definite  influence  on  the 
quality  and  level  of  care  that  is  being 
delivered.  Despite  their  protests  to  the 
contrary,  I believe  the  PROs  have 
come  down  harder  on  the  rural  physi- 
cians than  they  have  on  the  remainder 
of  us.  This  makes  rural  practice  less  at- 
tractive. Organized  medicine  must 
fight  for  the  right  of  all  physicians. 

The  federal  government's  push  to 
impose  DRGs  (Diagnostic  Related 
Groups)  on  our  radiologists, 
anesthesiologists,  and  pathologists  was 
correctly  seen  by  all  of  organized 
medicine  as  an  entering  wedge  that,  if 
successful,  would  ultimately  be  ap- 
plied to  all  physicians.  State  medical 
society,  specialty  society,  and  AMA 
(American  Medical  Association)  op- 
position was  successful.  Organization 


24  JOURNAL  VOL  140  JUNE 


in  this  instance  was  the  key.  The  future 
holds  more  government  interference; 
we  need  to  be  organized  and  ready  to 
combat  any  further  government  intru- 
sions into  the  practice  of  medicine. 

THE  FUTURE  QUALITY  OF  MEDICINE  is 

brighter  this  year  in  Louisiana  because 
of  a re-invigorated  State  Board  of 
Medical  Examiners  working  with  a 
strengthened  Medical  Practice  Act.  We 
do  not  need  physicians  in  our  ranks 
whose  acts  discredit  all  of  medicine. 
The  Louisiana  Board  of  Medical  Ex- 
aminers now  has  an  enhanced  ability 
to  effectively  "disbar"  these  in- 
dividuals. Is  there  a downside  to  this? 
Surely  there  is.  But  fortunately  the  Loui- 
siana Psychiatric  Association  and  the 
Board  of  Medical  Examiners  are 
cooperatively  working  on  rules  to  im- 
plement our  revised  Medical  Practice 
Act.  These  rules  will  preserve  physi- 
cians' individual  rights  as  well  as  leave 
the  Board  the  strength  to  deal  with  pro- 
blems. The  Louisiana  State  Medical 
Society  acted  as  a catalyst  between 
these  two  organizations.  Such  a role  is 
a fertile  field  for  further  activity  on  the 
part  of  the  LSMS.  I believe  the  future 
will  bring  greater  understanding  and 
cooperation  between  our  varied 
medical  organizations. 

The  election  of  Jerry  Thomas,  MD 
as  a state  representative  shows  what  a 
talented  and  determined  physician  can 
do  with  a little  help  from  the  LAMPAC 
(Louisiana  Medical  Political  Action 
Committee).  LAMPAC  also  stirred  up 
physician  support  for  Governor-elect 
Buddy  Roemer  with  its  "Coffee  with 
Representative  Roemer"  held  at  last 
year's  Annual  Meeting.  Physicians 
gave  an  identifiable  $300,000  to  the 
Roemer  campaign,  and  then  con- 
tributed generously  to  his  transition 
team.  We  have  every  reason  to  believe 
that  medicine  will  have  a more  recep- 
tive state  government  to  work  with.  We 
know  that  our  legislative  efforts  are 
conducted  on  behalf  of  our  patients 
and  good  government  in  general.  But 
persuading  the  often  hostile  Health  and 
Welfare  Committees  and  then  a less- 
than-receptive  Senate  and  House  has 


been  increasingly  difficult  in  the  past 
few  years.  We  hope  the  situation  will 
improve  with  the  anticipated  change  in 
legislative  leadership  and  membership. 
The  need  for  improvement  is  a necessi- 
ty, especially  as  we  witness  the 
paraprofessionals  attempting  to 
legislatively  extend  their  turf  into  the 
realm  of  medicine.  The  Optometry  Bill 
last  year  would  have  legalized  the 
treatment  of  disease  by  optometrists.  It 
would  have  defined  the  additional 
education  necessary  to  qualify  under 
the  law.  We  know  the  optometrists  are 
not  going  to  give  up  their  efforts.  Their 
defeat  last  year  only  came  after  ex- 
haustive opposition  orchestrated  by 
our  Office  of  Governmental  Affairs. 
Sharon  Knight  and  her  staff  deserve  a 
lot  of  credit.  Other  equally  onerous 
bills  are  coming.  We  need  a fair  shake 
from  our  state  government,  and  this 
time  I think  we're  going  to  get  it. 

I believe  greater  cooperation  bet- 
ween such  groups  as  the  American 
Association  of  Retired  Persons  (AARP) 
is  in  our  future.  This  is  desirable  and 
will  benefit  both  medicine  and  a large 
and  growing  segment  of  our  patient 
population.  We  have  many  similar 
goals  that  will  be  more  attainable  when 
coordinated  with  each  other.  J.D.  Mar- 
tin of  Baton  Rouge  is  responsible  for 
having  me  speak  at  a recent  AARP  state 
board  meeting.  I came  away  with 
good,  strong  vibes. 

IN  THE  AREA  OF  MEDICAL  LIABILITY  in- 
surance, I would  say  the  future  is  good 
for  its  availability  to  the  physicians  of 
Louisiana.  We  are  fortunate  in  having 
insurers  such  as  LAMMICO  (Louisiana 
Medical  Mutual  Insurance  Company), 
St  Paul,  the  Insurance  Corporation  of 
America,  and  Medical  Protective.  This 
last  company  came  here  in  June  of 
1 986  because  of  our  favorable  medical 
tort  laws  dating  back  to  Act  817  of 
1975.  We  are  fortunate  to  have  quali- 
ty companies  willing  to  do  business  in 
Louisiana.  Availability,  then,  is  not  a 
major  problem  for  most  of  our 
physicians. 

We  do  have  an  affordability  pro- 
blem. Despite  the  fact  that  our  liabili- 


ty coverage  costs  in  Louisiana  are  less 
than  that  in  two-thirds  of  all  states,  we 
have  some  problems.  These  insurance 
costs  are  great  enough  to  raise  the  cost 
of  patient  care,  change  practice  pat- 
terns, and  drive  needed  physicians  out 
of  practice.  Physicians  who  have  small 
practices  ...  whether  due  to  physical 
impairment,  age,  and/or  the  need  to 
slow  down,  or  who  practice  in  im- 
poverished communities  where  pa- 
tients are  unable  to  pay  the  customary 
fees  ...  simply  cannot  afford  to  pay 
liability  costs.  Concerned?  You  bet! 
What  is  the  Louisiana  State  Medical 
Society  doing  about  it,  and  what  does 
the  future  hold?  In  cooperation  with 
LAMMICO,  we  are  playing  an  active 
role  in  establishing  rules  for  our  at- 
torney general's  office  and  our  com- 
missioner of  insurance  to  follow  in 
their  administration  of  our  Patient's 
Compensation  Fund  (PCF).  The  fund 
has  not  been  run  as  efficiently  as  we 
believe  it  should.  I predict  that  it  will 
be,  once  these  rules  are  established. 
Some  drain  on  our  PCF  is  caused  by 
laws  such  as  one  passed  several  years 
ago  by  the  trial  attorneys  that  allows  ac- 
tion by  a plaintiff  against  the  PCF,  even 
if  the  defendant  settles  for  less  than 
$100,000.  Wrong?  Yes,  it  is;  but  I 
predict  that  we  can  pass  legislation  to 
correct  it.  Other  tort  laws  that  are  not 
medical  in  nature  run  up  the  cost  of  all 
liability  coverage,  medical  included. 
The  Collateral  Source  Rule  prevents 
the  court  from  knowing  about  previous 
payments  and  settlements  to  the  plain- 
tiff on  the  same  issue.  Our  joint  and 
several  law  was  modified  in  the  last 
legislature  - favorably  modified  - but 
still  allows  a defendant  with  only  507o 
of  the  fault  to  be  forced  to  pay  the  en- 
tire judgement.  I predict  that  these  can 
and  will  be  corrected  legislatively  by 
the  Louisiana  State  Medical  Society  in 
cooperation  with  the  business 
community. 

Iberia  Parish  Medical  Society  has 
a late  resolution  that  I hope  will  be  ac- 
cepted by  our  House  of  Delegates.  This 
is  a resolution  to  establish  an  En- 
vironmental Committee.  This  may  be 
the  key  to  finding  out  why  Louisiana 


JOURNAL  VOL  140  JUNE  25 


has  the  highest  cancer  rate  second  on- 
ly to  New  Jersey  in  the  50  states.  Our 
patients  are  aware  of  this  problem,  we 
are  aware  of  this  problem,  and  our 
good-faith  efforts  to  correct  it  will  be 
appreciated  by  the  public.  I predict 
Louisiana  will  be  an  even  better  place 
to  live  in  the  future. 

Many  of  us  think,  perhaps  with 
some  good  reason,  that  public  educa- 
tion on  health  issues  has  only  resulted 
in  lots  of  time  being  wasted  explaining 
things  that  formerly  we  did  not  have  to 
explain.  Sober  reflection  leads  me  to 
believe,  however,  that  education  has 
got  to  be  good  if  it  is  leavened  by  com- 
mon sense.  Public  concern  about  ill- 
understood  issues  manifests  itself  in 
our  mandatory  pre-marital  AIDS  (Ac- 
quired Immune  Deficiency  Syndrome) 
testing  law  ...  a boondoggle  if  there 
ever  was  one. 

Education  should  bean  important 
part  of  our  practice  of  medicine. 
Recognition  by  physicians  and  patients 
alike  of  self-destructive  habits  and 
lifestyles  has  already  reduced  our 
smoking  population.  Another  example: 
a recent  study  showed  that  the  simple 
distribution  of  an  elemental  book  on 
health  to  a group  of  welfare  recipients 
decreased  physician  visits  by  16%.  In- 
terest in  health  issues  has  never  been 
so  high.  We  physicians  need  to  be 
even  more  involved  in  education  and 
promulgation  of  information  that  is 
beneficial  to  our  patients'  health.  One 
test  of  a true  professional  is  one  who 
strives  to  decrease  the  problems  that 
create  the  need  for  his  or  her  services. 
Dentists  and  their  persistent  teaching 
of  the  benefits  of  proper  dental  hygiene 
provide  an  example  we  could  and 
should  make. 

Many  of  medicine's  problems  are 
those  of  society.  Breakdown  in  family 
life  with  an  increase  of  "latchkey 
children"  as  well  as  one-parent  families 
are  bound  to  increase  physical  illness 
as  well  as  that  increasing  army  of  the 
"worried  well." 

I AM  NOT  SO  NAIVE  AS  TO  BELIEVE  that 
medicine  can  cure  all  of  society's  ills, 
nor  that  society  can  cure  medicine's 


problems.  But  as  profesionals  who 
generally  are  held  high  in  esteem  by 
our  fellow  citizens,  we  do  bear  a cer- 
tain responsibility.  We  must  be  integral 
members  of  our  communities,  willing 
to  offer  our  expertise  and  experience 
to  address  the  present  and  future  needs 
of  our  patients,  communities,  and  na- 
tion. The  key,  I believe,  is  to  remain 
strong  as  a profession,  and  to  work 


diligently  against  unwarranted  and 
unacceptable  intrusions  into  the  prac- 
tice of  medicine.  We  must  never  lose 
sight  of  the  fact  that  we  are  our  pa- 
tients' best  health  care  advocates.  Our 
cohesiveness  will  improve  our  effec- 
tiveness in  helping  to  shape  social 
changes  that  can  provide  the  people 
we  serve  with  a better  quality  of  life. 


26  JOURNAL  VOL  140  JUNE 


The  LSMS  honors  its  50-year  doctors 


Pictured  above: 

1 . John  C.  Crenshaw  Jr,  MD,  Shreveport 

2.  Louis  A.  Breffeilh,  MD,  Shreveport 

3.  Joseph  M.  Brocato,  MD,  Baton  Rouge 

4.  Henry  C.  Voorhies  Jr,  MD,  Lafayette 

5.  Joseph  A.  Sabatier  Jr,  MD,  New  Orleans 

6.  Collins  P.  Lipscomb,  MD,  Pontchatoula 

7.  David  W.  Vangelder,  MD,  Baton  Rouge 

8.  John  L.  Kron  Jr,  MD,  New  Orleans 

9.  Myron  A.  Walker,  MD,  Baton  Rouge 

10.  Charles  L.  Black,  MD,  Shreveport 

1 1 . Oscar  D.  Thomas,  MD,  Thibodaux 

12.  Joe  E.  Holoubek,  MD,  Shreveport 

13.  Alice  B.  Holoubek,  MD,  Shreveport 

14.  John  M.  Cobb,  MD,  Shreveport 

15.  Joe  D.  Talbot,  MD,  Shreveport 

16.  Daniel  W.  Goldman,  MD,  New  Orleans 
1 7.  David  S.  Malen,  MD,  Baton  Rouge 

18.  Salvatore  J.  Cali,  MD,  Hammond 


Not  pictured: 

A.  Stirling  Albritton,  MD,  Baton  Rouge 
John  L.  Dileo,  MD,  New  Orleans 
Homer  J.  Dupuy,  MD,  New  Orleans 
James  H.  Eddy  Jr,  MD,  Shreveport 
Frederick  Eigenbrod,  MD,  New  Orleans 
Allan  M.  Goldman,  MD,  New  Orleans 
Bernard  A.  Goldman,  MD,  Harvey 
Joseph  P.  Griffon,  MD,  Baton  Rouge 
N.  Leon  Hart,  MD,  New  Orleans 
Robert  G.  Heath,  MD,  New  Orleans 
Jack  R.  Jones,  MD,  Baton  Rouge 
William  Locke,  MD,  New  Orleans 
J.  Morgan  Lyons,  MD,  New  Orleans 
Edward  W.  Nelson,  MD,  New  Orleans 
Luis  R.  Oms,  MD,  Metairie 
Louis  J.  Supple,  MD,  Franklin 
James  E.  Toups,  MD,  Summit,  MS 


JOURNAL  VOL  140  JUNE  27 


4 


1988-89  ELECTED  OFFICIALS 


President 
President-Elect 
Vice  President 
Immediate  Past  President 
Speaker,  House  of  Delegates 
Vice-Speaker,  House  of  Delegates 
Secretary-Treasurer 


EXECUTIVE  COMMITTEE 

Daniel  H.  Johnson  Jr,  MD,  New  Orleans 
Milton  C.  Chapman,  MD,  Shreveport 
John  C.  Cooksey,  MD,  Monroe 
James  W.  Vildibill  Jr,  MD,  Lafayette 
Samuel  A.  Leonard,  MD,  Metairie 
R.  Bruce  Williams,  MD,  Shreveport 
Howard  A.  Nelson  Jr,  MD,  Marrero 


Board  of  Councilors  6th  District:  Charles  D.  Belleau,  MD  (Chairman),  Baton  Rouge 

1 St:  Ronald  J.  French,  MD,  New  Orleans 
2nd:  Frank  J.  George,  MD,  Metairie 
3rd:  Philip  A.  Robichaux  Jr,  MD,  Raceland 
4th:  James  R.  Bergeron,  MD,  Shreveport 
5th:  David  M.  Walsworth,  MD,  West  Monroe 
7th:  G.  Michael  Kent,  MD,  Lake  Charles 
8th:  Leo  L.  Lowentritt  Jr,  MD,  Alexandria 
9th:  Emile  K.  Ventre  Jr,  MD,  Opelousas 
10th:  Stanford  A.  Owen,  MD,  Slidell 


Chairman,  Council  on  Legislation  Wallace  H.  Dunlap,  MD,  Baton  Rouge 


Delegates 


Alternates 


AMA  Delegates  Emeriti 


Young  Physicians  Section 


AMA  DELEGATION 

Robert  L.  diBenedetto,  MD,  Baton  Rouge 
Daniel  H.  Johnson  Jr,  MD,  New  Orleans 
A.G.  Kleinschmidt  Jr,  MD,  Marrero 
Donald  J.  Palmisano,  MD,  New  Orleans 
Eugene  F.  Worthen,  MD,  Monroe 
Terrence  Beven,  MD,  Baton  Rouge 
Samuel  A.  Leonard,  MD,  Metairie 
Conway  S.  Magee,  MD,  Lake  Charles 
W.  Juan  Watkins,  MD,  Shreveport 
A.  Jay  Binder,  MD  (Resident),  New  Orleans 
Ralph  H.  Riggs,  MD,  Shreveport 
W.  Charles  Miller,  MD,  New  Orleans 
Gordon  W.  Peek,  MD,  Baton  Rouge 
Stephen  L.  Jolissaint,  MD,  Opelousas 


28  JOURNAL  VOL  140  JUNE 


Physicians  Recognition  Award 

Forty-nine  physicians  from  the  state  of  Louisiana  were  awarded  the  Physicians  Recognition  Award  [PRA]  during 
March,  1 988.  This  award  is  presented  by  the  American  Medical  Association  to  physicians  who  have  voluntarily 
completed  150  hours  of  continuing  medical  education  during  a consecutive  three-year  time  period.  Of  these 
150  hours,  at  least  60  must  be  in  AMA/PRA  Category  1.  These  forty-nine  individuals  are  presented  below. 


Abbeville 

Sydney  Harold  Crackower,  MD* 

Baton  Rouge 

Cecil  Noel  Bankston  Jr.,  MD 
Willie  Zachary  Bienvenu,  MD 
Cecil  W.  Lovell  III,  MD 

Brusley 

Frederick  Erwin  Hackley,  MD 

Donaldsonville 

Glenn  David  Schexnayder,  MD 

Franklin 

Brent  Wheeler  Allain,  MD 

Gonzales 

Richard  Anthony  Streb,  MD 

Gretna 

Thiem  Dang,  MD 

Harahan 

Fayez  H.  j.  Hadidi,  MD* 

Kinder 

John  James  Storer,  MD 


Lake  Charles 

Ralph  W.  Colpitts,  MD 
Randall  Coy  Duplechain,  MD 
Cliff  Charles  Laborde  Jr.,  MD 
Richard  Edward  Landry,  MD 

Lafayette 

Darrell  Lane  Henderson,  MD 
Andre  Keath  Perron,  MD 
T.  Ramakrishnan,  MD 

Metairie 

Gustavo  Alberto  Colon,  MD 
Robert  Merritt  de  Bellevue,  MD 
George  Gaethe,  MD 
Julian  H.  Sims,  MD 

Monroe 

Philip  Rand  Warren,  MD 

Morgan  City 

Robert  Paul  Blereau,  MD 

New  Orleans 

Albert  Barrocas,  MD 
Patrick  John  Dowling,  MD* 
George  Wilden  Hoffman,  MD 
Peter  Robert  KastI,  MD 
Donald  Robert  Lee  May,  MD* 
Patrick  Edward  Mottram,  MD 
A.  Mark  Parker  Jr.,  MD 
Carlos  D.  Restrepo,  MD* 
Frank  Adams  Riddick  Jr.,MD 
Raphael  Ross,  MD 
Beverly  Ann  B.  Yount,  MD 


Oakdale 

Ghanta  Madhusudan  Rao,  MD* 

Paradis 

Wilson  Paul  Couch,  MD 

Pontchatoula 

David  Wells  Bass,  MD* 


Shreveport 

Michael  O.  Fleming,  MD 
Erie  Warfield  Harris,  MD 
William  P.  Kinnebrew,  MD 
Don  Melvin  Morris,  MD 
Milton  Kenneth  Scharff,  MD 
Daniel  Richard  Stevenson,  MD 
John  Peter  Valiulis,  MD 

Slidell 

Richard  Emmett  Barlow,  MD 
Esteban  Oscar  Romano,  MD 

Ville  Platte 

Barney  J.  Fusilier,  MD 

West  Monroe 

Warren  Atwood  Daniel  Jr.,  MD 


* These  individuals  are  not  members  of  the  Louisiana  State  Medical  Society. 


JOURNAL  VOL  140  JUNE  33 


HEART  TRANSPLANTATION 

THE  LOUISIANA  EXPERIENCE 


JOHN  L OCHSNER,  MD;  CLEMENT  C.  EISWIRTH  JR,  MD 


34  JOURNAL  VOL  140  JUNE 


The  renewed  Louisiana  experience  in  cardiac 
transplantation  now  spans  more  than  two  years. 
During  this  period,  27  patients  have  received 
transplanted  hearts.  Improved  measures  in 
immunology,  organ  preservation,  and  the  detection 
and  treatment  of  rejection  have  favorably  affected 
the  outcome.  The  results  in  this  experience  are 
exceptionally  good.  There  is  a 93%  one-year 
survival  and  in  each  patient  the  cardiac  status  has 
reverted  to  New  York  Heart  Association  Class  I. 
The  expectation  of  excellent  long-term  survival 
warrants  continued  efforts  to  treat  selected  patients 

in  end-stage  heart  disease. 


ONE  OF  THE  most  spectacular  medical  achievements 
was  in  1967,  when  Dr.  Christian  Barnard  re- 
ported the  first  successful  human  cardiac  transplan- 
tation.^ In  the  next  few  years,  we  and  many  centers 
performed  either  isolated  or  a limited  number  of  car- 
diac transplants.  This  early  experience  was  disap- 
pointing since  the  majority  of  patients  died  within  the 
first  post-transplant  year.  Hence,  the  procedure  was 
considered  experimental  and,  except  for  the  contin- 
ued efforts  by  the  Stanford  University  and  the  Medical 
College  of  Virginia  groups,  the  medical  profession 
self-proclaimed  a moratorium  on  cardiac  transplan- 
tation. However,  since  1982,  there  has  been  a re- 
newed interest  in  the  procedure  due  to  significant 
advances  in  immunosuppression,  patient  selection, 
myocardial  preservation,  diagnosis  of  rejection,  and 
a better  understanding  of  patient  management.  Uti- 
lizing these  advances,  more  and  more  institutions  have 
re-entered  or  initiated  programs.  Today  there  are  84 
cardiac  transplantation  centers  in  the  United  States 
and  more  than  30  in  other  countries.  There  were  800 
cardiac  transplantations  performed  in  1985  with  cur- 
rent statistics  indicating  an  80%  one-year  survival  and 
70%  two-year  survival.^  The  Ochsner  Clinic  renewed 
its  cardiac  transplantation  program  on  September  4, 
1985,  and  the  first  transplant  was  performed  on  Oc- 
tober 30,  1985.  The  stimulus  for  development  of  the 
program  was  determined  by  a definite  need  for  a car- 
diac transplantation  center  in  our  geographic  region. 
The  ability  to  institute  this  program  was  a natural 
extension  of  an  established  kidney  and  bone  marrow 
transplantation  program  and  an  ongoing  active  multi- 
faceted open-heart  program. 


^4^  JAble  1 

CRITERIA  FOR  ELIGIBILITY  AS  A CARDtS; 
TRANSPLANT  RECIPIENT 


1.  Severe,  Class  ill  or  IV  cardiac  dysfunction  unremedial  to 
surgical  treatment  other  than  cardiac  replacement 

2.  Limited  life  expectancy,  with  a one-year  mortality  estimated 
to  be  > 50% 

3.  Physiologic  age  < 60  years;  absolute  upper  limit  for 
chronologic  age  is  65 

4.  No  systemic  illness  other  than  abnormalities  related  to 
heart  failure 

5.  Emotional  stability 

6.  Strong  family  support  system 

7.  Absence  of  the  following  exclusion  criteria: 

a.  Severe  pulmonary  hypertension  (PVR  > 8 wood  units 
or  PVR  > 6 wood  units  with  inability  of  nitroprusside 
infusion  to  reduce  PVR  to  below  3 or  inability  to 
reduce  PA  systolic  below  50  mmHg 

b.  Severe,  irreversible  hepatic,  renal  or  pulmonary 
disease 

c.  Active  systemic  or  pulmonary  infection 

d.  Recent  pulmonary  infarction 

e.  Insulin-dependent  diabetes 

f.  History  of  uncontrollable  hypertension,  defined  as 
blood  pressures  consistently  greater  than  160/100  mm/ 
Hg  on  medical  therapy 

g.  Systemic  vascular  or  cerebral  vascular  disease 

h.  Active  peptic  ulcer  disease 

i.  History  of  substance  abuse  (including  alcohol)  or 
behavior  problem 


PVR:  pulmonary  vascular  resistance 
PA:  pulmonary  artery 


CLINICAL  DATA 

We  have  received  numerous  phone  calls  on  behalf  of 
potential  recipients.  Screening  at  this  level  determines 
the  suitability  of  the  patient,  resulting  in  a higher 
acceptance  percentage  of  patients  actually  referred. 
The  criteria  for  acceptance  are  shown  in  Table  1.  Fifty- 
seven  patients  have  been  referred  for  cardiac  trans- 
plantation (Table  2),  16  of  which  were  rejected.  Rea- 
sons for  exclusion  are  listed  in  Table  3.  One  patient 
who  would  have  been  an  acceptable  candidate  based 
upon  initial  screening  declined  further  consideration 
and  was  lost  to  followup.  One  patient  had  a history 
of  being  a recovered  alcoholic  who  had  joined  Alco- 
holics Anonymous  and  gained  the  support  of  his  fam- 
ily. He  was  rejected  because  of  a brachial  cleft  fistula 
which  prevented  sterile  entry  into  the  right  jugular 
vein.  Due  to  technical  difficulty,  alternative  biopsy 


JOURNAL  VOL  140  JUNE  35 


TABLE  2 

CARDIAC  TRANSPLANTATION  — 

PATIENT  PATTERN 

Referred  for  transplantation 

57 

Rejected  (medical  and  social) 

16 

Died  awaiting  transplant 

2 

Received  transplantation 

27 

Awaiting  transplantation 

12 

routes  are  not  amenable  to  the  repeated  entries  nec- 
essary to  obtain  multiple  biopsy  specimens.  Since  this 
is  so  important  for  adequate  management  of  the  car- 
diac transplant  patient,  he  was  rejected. 

Two  additional  patients  died  while  awaiting 
transplantation,  one  of  cardiogenic  shock  after  being 
transferred  for  emergent  cardiac  transplantation  when 
no  donor  could  be  located,  and  the  other  of  congestive 
heart  failure  following  a pulmonary  embolus  which 
had  made  him  an  unsuitable  candidate. 

Twenty-seven  patients  have  undergone  cardiac 
transplantation.  There  were  22  males  and  5 females, 
and  their  ages  ranged  from  12  to  60  (mean  45.2,  me- 
dian 48).  The  primary  cardiac  diseases  in  these  pa- 
tients were  as  follows:  ischemic  cardiomyopathy  in 
14,  idiopathic  cardiomyopathy  in  10,  congenital  heart 
disease  in  2 and  rheumatic  valvular  cardiomyopathy 
in  1. 

The  referrals  have  come  from  a wide  base  in- 
cluding Texas,  Mississippi,  and  Alabama.  Of  the  27 
patients  receiving  transplants,  19  (70.4%)  were  from 
Louisiana,  6 (22.2%)  from  Mississippi,  and  2 (7.4%) 
from  Alabama.  All  patients  were  in  New  York  Heart 
Association  Classification  III  or  IV. 

Donor  hearts  were  obtained  from  many  different 
locations  in  five  states.  The  ischemic  time  ranged  from 
59  minutes  to  three  hours  and  14  minutes  (average 
one  hour  and  54  minutes). 

A careful  surgical  and  medical  evaluation  was 
done  on  all  patients.  Two  patients  were  on  intra-aortic 
balloon  counterpulsation  in  order  to  maintain  suffi- 
cient hemodynamics  to  transport  them  to  the  oper- 
ating room.  Four  hospitalized  patients  required  vaso- 
active drug  infusions  to  stay  alive.  Two  patients  had 
cardiac  arrest  during  the  induction  of  anesthesia  and 
were  immediately  placed  on  extracorporeal  circula- 
tion. 


TABLE  3 

REASONS  FOR  EXCLUSION  FROM 
CARDIAC  TRANSPLANTATION 


Pulmonary  hypertension  2 

Diabetes  2 

Severe  peripheral  vascular  disease  2 

Poor  medical  compliance  2 

Poor  social  support  2 

Substance  abuse  2 

Active  infection  1* 

Cerebrovascular  accident  (recent)  1 * 

Severe  systemic  hypertension  1 

Inability  to  biopsy  1 

Patient  declined  1 


* Same  patient 


In  addition  to  the  transplantation  medical  and 
surgical  teams,  these  patients  were  evaluated  by  clin- 
ical psychiatry,  nursing,  social  services,  and  pastoral 
service.  Of  the  27  patients  receiving  transplants,  25 
were  listed  on  national  computer  systems  to  await  a 
suitable  donor. 

Immunosuppressive  therapy  varied  according  to 
the  patient's  individual  problems  and  the  availability 
of  drugs.  In  general,  two  different  protocols  have  been 
followed.  In  both  protocols,  triple  drug  therapy  con- 
sisting of  cyclosporin,  azathioprine  (Imuran®),  and 
steroids  was  used.  In  one  group,  the  use  of  antilym- 
phocyte globulin  in  the  preoperative  and  early  post- 
operative period  was  added  to  this  triple  therapy.  In 
general,  cyclosporin  levels  are  maintained  above  75 
ng/mL,  as  measured  by  high  pressure  liquid  chro- 
matoptometry  technique.  Imuran®  is  progressively 
lowered  to  a daily  maintenance  dose  of  1.0  mg/kg  to 
2.0  mg/kg,  and  prednisone  is  tapered  to  a mainte- 
nance dose  of  0.1  mg/kg  to  0.15  mg/kg. 

All  patients  have  undergone  repeated  endomy- 
ocardial biopsies.  These  are  scheduled  every  week  for 
the  first  six  weeks,  then  every  two  weeks  for  the  next 
six  weeks,  then  every  month  for  three  months,  then 
every  two  months  for  six  months,  and  every  three 
months  thereafter. 

RESULTS 

Twenty-seven  patients  have  received  transplants  with 


36  JOURNAL  VOL  140  JUNE 


a followup  of  one  week  to  25.5  months  (mean  9.4 
months).  There  have  been  no  operative  deaths  and 
only  two  late  deaths  (Fig).  The  first  death  was  in  a 
12-year-old  boy  who,  in  his  sixth  month  following 
transplantation,  developed  gastroenteritis  and  during 
a three-day  period  was  unable  to  maintain  his  oral 
intake  of  immunosuppressive  drugs.  He  had  an  acute 
rejection.  He  arrived  at  the  hospital  in  cardiogenic 
shock  and  required  extracorporeal  membrane  oxy- 
genation to  maintain  life.  His  rejection  was  reversed 
with  steroid  and  antilymphocyte  globulin.  He  devel- 
oped fatal  disseminated  aspergillosis  with  extensive 
central  nervous  system  involvement.  The  other  death 
occurred  in  a man  who  developed  Pneumocystis  carinii 
pneumonia  two  months  following  transplantation.  He 
subsequently  developed  disseminated  cytomegalo- 
virus infection,  bacterial  sepsis,  and  renal  failure  and 
died  30  days  after  presentation  with  infection.  The 
remaining  25  patients  are  alive.  Thus,  the  actuarial 
one-year  survival  in  this  series  is  93% . 

Fourteen  patients  have  been  followed  for  six 
months  to  25.5  months  (mean  16.2  months,  median 
16.5  months).  Of  these  patients,  only  the  12-year-old 
died.  While  it  is  too  early  to  project  a meaningful  two- 
year  survival,  these  data  suggest  that  mortality  be- 
yond six  months  may  not  increase  substantially  though 
a longer  followup  wiU  be  needed.  This  is  consistent 
with  the  reports  of  the  Transplant  Registry. 

Complications  have  been  relatively  few.  Two  pa- 
tients developed  superficial  wound  infections  (one 
chest  and  one  groin)  requiring  open  drainage  with 
subsequent  healing  by  secondary  intention.  One  week 
postoperatively,  one  patient  developed  an  episode  of 
cerebral  ischemia  which  spontaneously  resolved.  An- 
other patient  remains  in  the  hospital  without  the  need 
of  support,  but  with  significant  cerebral  impairment. 
During  the  postoperative  period,  five  patients  devel- 
oped oral  candidiasis  and/or  herpes  simplex,  all  of 
which  resolved  within  the  first  month.  Three  patients 
developed  herpes  zoster,  two  with  a single  derma- 
tome and  one  with  multiple  dermatome  involvement. 
Atrial  fibrillation  required  treatment  in  two  patients. 
There  were  two  hemodynamically  significant  epi- 
sodes of  rejection  and  one  pulmonary  embolus.  There 
were  three  serious  infections:  one  patient  with  dis- 
seminated aspergillosis  and  two  patients  with  pneu- 
monia. 

REJECTION 

Cardiac  rejection  is  generally  termed  mild  if  only  peri- 


Fig.  Length  of  followup  of  27  cardiac  transplant 
recipients. 


Number  of  months 


vascular  infiltrates  are  present,  moderate  if  there  is 
interstitial  extension,  and  severe  if  the  infiltrate  is  ex- 
tensive and  mycotic  necrosis  is  present  within  the 
areas  of  the  infiltrates.  With  the  use  of  cyclosporin, 
many  patients  develop  cardiac  fibrosis  (which  is  not 
clinically  relevant)  and  lymphocytic  perivascular  in- 
filtrates without  clinical  sequelae.  For  this  reason,  most 
programs  only  treat  patients  who  develop  interstitial 
extension  unless  clinical  features  suggest  the  need  to 
treat  a lesser  degree  of  infiltration. 

Cardiac  rejection  is  most  frequent  within  the  first 
six  months  following  transplantation.  In  our  series, 

14  patients  followed  for  at  least  six  months  developed 
18  rejections  for  an  average  of  1.3  rejections/patient. 
Only  two  patients  demonstrated  rejection  after  the 
first  six  months.  One  of  these  is  a poorly  compliant  ► 

JOURNAL  VOL  140  JUNE  37 


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REMEMBER  TO  WRITE  “DO  NOT  SUBSTITUTE.” 
IT  PROTECTS  YOUR  DECISION. 


Copyright  © 1987  by  Roche  Products  Inc.  All  rights  reserved. 


The  cut  out  "V"  design  is  a registered  trademark  of  Roche  Products  Inc. 


patient  who  has  had  a total  of  three  rejections,  with 
two  of  these  occurring  seven  months  and  17  months 
following  transplantation.  The  other  patient  had  no 
rejections  within  the  first  year  following  transplan- 
tation but  subsequently  developed  three  episodes. 
Both  are  currently  without  rejection  at  18.5  months 
and  16.5  months  of  followup,  respectively. 

Overall,  the  27  patients  have  developed  32  epi- 
sodes of  rejection.  This  yields  1.2  episodes  of  rejec- 
tion/patient with  a mean  followup  of  9.4  months,  me- 
dian 6.0  months. 

All  patients  who  received  transplants  are  now 
New  York  Heart  Association  Class  I.  Many  have  re- 
turned to  their  previous  occupations  or  are  receiving 
retraining  in  another  occupation.  Three  patients  have 
moderate  degrees  of  renal  insufficiency  with  serum 
creatinines  of  1.7  mg%  to  2.2  mg%.  All  but  three 
patients  have  developed  hypertension  secondary  to 
cyclosporin  and  are  receiving  antihypertensive  ther- 
apy. 

DISCUSSION 

Over  3,000  heart  transplants  have  been  performed 
worldwide.  More  than  one-half  of  these  were  per- 
formed in  the  past  two  years.  The  effects  of  trans- 
plantation on  quality  of  life  can  be  dramatic.  In  terms 
of  cardiac  status,  improvement  from  New  York  Heart 
Association  Class  III-IV  clinical  condition  to  Class  I 
has  occurred  in  all  our  patients.  Transplanted  hearts 
have  demonstrated  excellent  function.  Despite  de- 
nervation, the  heart  displays  normal  contractility  and 
contractile  reserve. 

The  limitations  placed  on  isolation  of  recipients 
has  become  more  lenient  as  experience  increases  and 
results  improve.  The  age  of  recipients  has  progres- 
sively increased  and  the  late  survival  for  patients  50 
to  65  years  of  age  is  similar  to  that  of  patients  under 
50  years  of  age. 

Today,  the  national  one-year  survival  is  80%  and 
the  two-year  survival  is  65%.  The  survival  of  our  pa- 
tients has  been  excellent.  A total  of  91%  have  survived 
one  year.  Our  two-year  survival  rate  will  require  a 
longer  followup.  Thus  far,  all  patients  surviving  six 
months  following  cardiac  transplantation  remain  alive 
at  followup  of  six  months  to  25.5  months  (mean  16.2 
months,  median  16.5  months).  A close  interrelation- 
ship of  all  concerned  in  the  various  stages  of  the  care 
of  these  extraordinarily  complicated  patients  is  essen- 


tial to  a successful  outcome.  The  selection  and  prep- 
aration of  recipients,  the  procurement  of  the  donor 
organs,  the  operative  implantation  of  the  organs,  and 
the  immediate  and  late  postoperative  therapy  should 
be  synchronized  in  order  to  achieve  maximum  ben- 
efit. A full-time  cardiac  transplantation  service  best 
meets  these  needs,  and  frequent  conferences  which 
include  all  members  of  the  team  serve  to  communicate 
the  essential  requirements  of  various  members  and 
their  patients. 

In  the  early  days  of  transplantation  when  im- 
munosuppression relied  on  multiple  courses  of  high- 
dose  steroid  therapy,  patients  were  vulnerable  to  an 
extremely  high  rate  of  infection.  The  advent  of  cy- 
closporin and  its  immunosuppressive  efficacy  has  been 
a- major  breakthrough  in  the  prevention  of  life-threat- 
ening infections.  Moreover,  the  knowledge  gained  in 
the  use  of  many  different  immunologic  agents  has  led 
to  a better  understanding  of  patient  management.  The 
use  of  multiple  agents,  combined  in  such  a manner 
as  to  maintain  patients  on  a dosage  of  each  drug  low 
enough  to  not  excite  complications,  has  allowed  long- 
term survival  without  increased  hazards  from  the 
drugs.  The  continued  development  of  new  drugs 
combined  with  a better  knowledge  of  immunology 
should  continue  to  provide  better  means  to  control 
rejections. 

Monitoring  the  immune  system  by  way  of  pe- 
ripheral blood  is  a useful  support  mechanism  for  car- 
diac transplantation.  Immune  monitoring  with  mono- 
clonal antibodies  and  flow  cytometry  may  be  useful 
as  an  adjunct  study  in  the  early  diagnosis  of  infection, 
allograft  rejection,  and  malignant  clonal  proliferation 
of  B cells.  We  have  observed  that  up  to  two  weeks 
before  an  allograft  rejection  occurs,  peripheral  blood 
lymphocyte  subsets  express  activation  antigens  such 
as  the  transferrin  receptor.  Expression  of  activation 
antigens  on  the  peripheral  blood  lymphocytes  in  an 
immunosuppressed  cardiac  transplant  patient  greatly 
increases  the  risk  for  an  allograft  rejection  episode. 

An  increased  Helper  T/Suppressor  T ratio  (normal  1.8) 
also  increases  the  risk  of  a rejection  episode.  The 
T Helper  population  has  two  important  functional 
subsets:  1)  the  helper  inducer  subset,  which  is  im- 
portant in  regulating  activation  of  the  immune  sys- 
tem; and  2)  the  suppressor  inducer  subset,  which  is 
important  in  regulating  suppressor  effector  activity  of 
the  immune  system.  We  have  observed  a relative  def- 
icit of  the  suppressor  inducer  subset  during  rejection  ► 

JOURNAL  VOL  140  JUNE  39 


ACKNOWLEDGMENTS 


episodes  but  not  during  infection  episodes.  During 
viral  infection,  we  have  observed  a severely  decreased 
Helper  T/Suppressor  T ratio  together  with  a signifi- 
cant HLA-DR  activation  of  T cells.  One  may  expect 
to  see  a significantly  increased  Helper  T/Suppressor 
T ratio  during  bacterial  infections,  especially  Staphy- 
lococcus infections.  For  the  future,  we  can  anticipate 
that  monoclonal  antibodies  will  play  an  ever-increas- 
ing role  in  the  treatment  of  rejection  episodes.  The 
same  monoclonal  antibody  that  is  now  used  to  detect 
activated  lymphocyte  subsets  as  a means  for  early 
diagnosis  of  rejection  episodes  can  potentially  be  em- 
ployed in  the  treatment  of  cardiac  transplant  recipi- 
ents. 

In  the  formulative  years  of  cardiac  transplanta- 
tion, the  methods  and  means  to  determine  rejection 
were  crude  and  inaccurate.  The  development  and  use 
of  endomyocardial  biopsy  has  proven  precise  in  the 
diagnosis  of  rejections.  Grades  of  rejection  and,  con- 
sequently, the  need  and  degree  of  therapy  can  be 
ascertained.  This  information  has  been  of  immeas- 
urable assistance  in  determining  the  need  for  treat- 
ment and  control  of  rejection. 

Newer  methods  of  myocardial  preservation  have 
helped  to  increase  the  supply  of  organs  by  allowing 
more  time  from  procurement  to  transplantation.  Thus 
logistics  have  improved  since  organs  can  travel  longer 
distances,  and  more  time  is  allotted  to  the  technical 
aspects  of  the  operation. 

In  conclusion,  the  first  two  years  of  renewed  car- 
diac transplantation  at  the  Ochsner  Clinic  have  dem- 
onstrated significant  activity.  Patient  survival  is  con- 
siderably better  than  the  national  average,  and  the 
rate  of  infection  and  rejection  is  likewise  well  con- 
trolled. The  recipients  have  been  able  to  return  to 
active  and  productive  lives.  This  successful  experi- 
ence warrants  continuation  of  this  endeavor.  ■ 


Many  individuals  have  participated  in  the  care  of  the 
cardiac  transplant  patients  and  we  wish  to  recognize 
some:  Dr  Clark  Springgate,  Dr  John  L.  Hussey,  Dr 
Walter  Culpepper,  Dr  Luther  Williams,  Dr  Nelson 
Ancalmo,  Dr  Noel  Mills,  Dr  Michael  Horowitz,  Dr 
John  Busby,  Dr  James  Gilmore,  Dr  Tommy  Fudge,  Dr 
Shannon  Cooper,  Dr  Donald  Harmon,  Dr  Robert  Mar- 
ino, Dr  Peter  Stedman,  Mr  Frank  J.  Heckenkemper, 
Mr  William  T.  Stevenson,  Miss  Ellen  Badeaux,  RN, 
and  Miss  Debi  Dumas,  RN. 

REFERENCES 

1.  Barnard  CN:  Human  cardiac  transplant:  An  interim  report  of  a successful 
operation  performed  at  Grote  Schuur  Hospital,  Cape  Town.  S Afr  Med  J 
1976;41:1271-1274. 

2.  Kaye  MP:  The  International  Heart  Transplantation  Registry,  1984  report. 
Heart  Transplantation  1985;4:290-292. 


Dr  Ochsner  is  from  the  Dept  of  Surgery  at  Ochsner  Clinic  and  Alton 
Ochsner  Medical  Foundation  in  New  Orleans. 

Dr  Eiswirth  is  from  the  Dept  of  Internal  Medicine,  Section  on 
Cardiology  at  Ochsner  Clinic  and  Alton  Ochsner  Medical  Foundation  in 

New  Orleans. 

Reprint  requests  should  be  sent  to  Dr  John  Ochsner,  Ochsner  Clinic, 
1514  Jefferson  Hwy,  New  Orleans,  LA  70121. 


40  JOURNAL  VOL  140  JUNE 


MICROSURGERY  IN  BREAST 
RECONSTRUCTION  USING  THE 
SUPERIOR  GLUTEUS  FOR 
FREE  TISSUE  TRANSFER: 

A CASE  REPORT 


MARY  LYN  T.  LU,  MD;  WILLIAM  M.  SWARTZ,  MD 


The  gluteus  free  flap  breast  reconstruction  is 
presented  as  an  alternative  to  other  methods, 
including  tissue  expands  and  the  transverse 
abdominal  flap.  The  principal  reasons  to  consider 
this  method  are  the  availability  of  adipose  tissue 
in  the  gluteal  region,  even  in  thin  patients,  and  the 
well-tolerated  donor  site.  The  authors'  preference 
for  early  reconstruction  is  based  on  data  which 
indicate  that  most  local  recurrences  do  not  occur 
until  after  the  accepted  two-year  interval. 


Breast  cancer  is  the  most  frequent  malignancy  in 
women,  with  a progressive  rise  in  incidence  after 
the  third  decade  of  life.  In  the  United  States  alone, 
approximately  40,000  radical  mastectomies  are  per- 
formed each  year.^ 

While  most  of  the  women  who  undergo  mastec- 
tomy are  able  to  adjust,  studies  have  shown  that  there 
is  a definite  psychological  effect  of  mastectomy.^  The 
four  most  common  categories  are  depression  lasting 
for  months  to  years,  lowered  self-esteem,  diminished 
sense  of  femininity,  and  panic  imposed  by  the  po- 
tentially lethal  cancer.  The  greatest  benefit  of  breast 
reconstruction  is  improving  the  patient's  sense  of  well 
being.  Restoration  of  the  breast  form  increases  the 
patient's  feelings  of  femininity,  decreases  self-con- 
sciousness and  embarrassment,  and  improves  overall 
appearance,  with  relief  from  clothing  and  prosthetic 
problems.^' 2 

The  timing  of  breast  reconstruction  varies  mostly 
due  to  physician  bias.  Immediate  reconstruction  at 
the  time  of  mastectomy  or  within  the  first  week  post- 
operatively  is  gaining  acceptance  in  Stage  I disease.^ 
Some  physicians  prefer  to  wait  two  years  with  the 
belief  that  80%  of  local  recurrence  develops  within 
two  years.  There  are  reports  in  the  literature^'  ^ that  a ► 

JOURNAL  VOL  140  JUNE  43 


two-year  delay  in  breast  reconstruction  is  not  justified 
and  is  without  oncologic  advantage  because  in  Stage 
I disease,  the  mean  disease-free  interval  is  6.2  years 
and  it  takes  10  years  for  80%  of  recurrences  to  ap- 
pear.^'^ Our  preference  is  to  perform  immediate  re- 
construction when  feasible.  Delayed  reconstruction  as 
soon  as  the  patient's  post-mastectomy  scars  are  soft- 
ened (usually  within  six  months  of  surgery)  is  a rea- 
sonable alternative  to  waiting  two  years.  For  patients 
undergoing  chemotherapy,  reconstruction  is  per- 
formed following  recovery  of  the  white  blood  count 
in  an  interval  between  treatments. 

CHOICE  OF  METHOD 

Recent  advances  in  breast  reconstruction  have  pro- 
vided a variety  of  methods  that  can  be  adapted  to 
each  patient's  needs. 

For  immediate  reconstruction,  the  most  fre- 
quently performed  procedure  is  the  tissue  expander, 
later  exchanged  for  a permanent  prosthesis  of  slightly 
smaller  size  at  a second  procedure.  Newer  permanent 
expanders  are  available,  thereby  obviating  a second 
procedure.  While  this  method  is  probably  the  easiest 
on  the  patient,  it  has  certain  drawbacks.  Frequently, 
it  is  not  possible  to  match  the  opposite  breast  in  size 
and  contour.  In  many  of  these  reconstructions,  cap- 
sular contractures  around  the  implant  necessitate  im- 
plant exchange  or  removal.  Finally,  adequate  soft  tis- 
sue coverage  may  not  be  present  in  patients  requiring 
wide  skin  excision. 

To  obviate  the  problems  associated  with  pros- 
thetic reconstruction  and  to  match  the  contralateral 
ptotic  breasts,  the  Transverse  Rectus  Abdominal  Mus- 
culocutaneous Flap  (TRAM),  based  on  the  superior 
epigastric  pedicle,  was  developed  by  Hartrampf.^  The 
TRAM  flap  provides  autogenous  tissue  with  an  ad- 
equate volume  for  the  largest  breast  mound  and  gives 
the  added  benefit  of  flattening  the  abdomen.  With 
this  procedure,  there  is  a possibility  of  weakening  the 
abdominal  wall  due  to  sacrifice  of  the  rectus  muscle. 
It  is  not  recommended  for  obese  patients  or  heavy 
smokers  and  may  be_ contraindicated  in  the  presence 
of  multiple  abdominal  scars  that  impair  blood  supply 
to  the  flap.  It  is  not  ideal  when  there  is  an  inadequate 
abdominal  panniculus  or  if  pregnancy  is  desired  at  a 
later  time. 

To  overcome  the  limitations  of  the  previous  pro- 
cedures, the  superior  gluteus  myocutaneous  flap  as 


Fig  1.  Preoperative  view.  Note  size  and  ptosis  of 


contralateral  breast. 


a free  tissue  transfer  was  first  reported  by  Fujino^  and 
later  refined  by  Shaw.®  The  superior  gluteus  myocu- 
taneous flap  provides  autogenous  tissue,  which,  like 
the  TRAM  flap,  is  soft  and  simulates  normal  breast 
tissue.  Even  in  thin  patients,  there  is  always  adequate 
tissue  for  breast  reconstruction  and  the  scar,  hidden 
from  the  patient's  normal  view,  is  cosmetically  ac- 
ceptable. Sacrifice  of  a portion  of  the  gluteus  muscle 
does  not  impair  function  of  the  remaining  muscle, 
and  the  contour  change  is  minimal.  Although  this  is 
a relatively  long  procedure  with  the  need  of  special 
facilities  and  microsurgical  techniques,  it  provides  a 
reliable  and  aesthetically  acceptable  reconstruction  in 
problem  patients. 

CASE  REPORT 

A 30-year-old  female  with  a Stage  I infiltrating  in- 
traductal carcinoma  had  a right  modified  radical  mas- 
tectomy. She  did  not  want  to  have  a prosthetic  re- 
construction. Her  abdomen  was  flat,  without  a good 
panniculus,  and  she  wished  to  become  pregnant  at  a 
later  time.  Six  months  post-mastectomy,  she  was  re- 
constructed with  a superior  gluteus  myocutaneous 
free  tissue  transfer.  The  superior  gluteal  artery  and 
vein  were  anastomosed  to  the  internal  mammary  ar- 
tery and  vein  with  a vein  interposition  graft.  Three 


44  JOURNAL  VOL  140  JUNE 


Fig  2.  Postoperative  view.  Nipple  areolar  complex 
reconstructed  with  quadripod  flap  and  free 
skin  graft.  Contralateral  breast  was  elevated 
with  a mastopexy. 


months  after  the  mound  reconstruction,  she  under- 
went a nipple  areola  complex  reconstruction  using  a 
quadripod  flap  for  the  nipple  and  a full-thickness  skin 
graft  for  the  areola.  The  left  breast  required  a mas- 
topexy for  final  symmetry  (Figs  1-3). 

SUMMARY 

Immediate  reconstruction  for  early  breast  cancer  has 
important  psychological  benefits  that  should  be  con- 
sidered in  the  patient's  overall  treatment  plan.  Per- 
forming a reconstruction  before  the  standard  two-year 
delay  has  not  been  shown  to  increase  the  incidence 
of  local  recurrence  or  hinder  its  detection  and  treat- 
ment.^' ^ 

There  are  several  options  in  breast  reconstruction 
with  individual  benefits  and  limitations.  An  autoge- 
nous breast  mound  with  adequate  volume  that 
matches  a ptotic  contralateral  breast  in  shape,  vol- 
ume, and  firmness  is  the  reconstructive  goal.  The  su- 
perior gluteus  mycocutaneous  free  tissue  transfer  is 
presented  as  a reasonable  alternative  to  the  transverse 
abdominal  island  flap. 

The  principal  advantage  lies  in  the  quality  of  the 
donor  site  which  is  most  acceptable  from  an  aesthetic 


Fig  3.  Donor  site  following  gluteus  myocutaneous 
flap  breast  reconstruction. 


and  functional  point  of  view.  For  patients  in  whom 
other  methods  of  reconstruction  are  neither  possible 
nor  acceptable,  the  gluteus  free  flap  breast  reconstruc- 
tion becomes  the  procedure  of  choice.  ■ 

REFERENCES 

1.  Coin  JM,  Coin  MK:  Changing  the  Body  — Psychological  Effects  of  Plastic 
Surgery.  Baltimore,  Williams  and  WUkms,  1981,  pp  163-189. 

2.  Snyderman  RK:  Reconstruction  of  the  Breast  After  Surgery  for  Malignancy, 
Goldwyn  RM  (ed).  Boston,  Little  Brown  and  Co,  1976;  pp  465-479. 

3.  Noone  RB,  Murphy  JB,  Spear  SL,  et  al;  A six-year  experience  with  im- 
mediate reconstruction  after  mastectomy  for  cancer.  Plast  Reconstr  Surg 
1985;76:258-269. 

4.  Dowden  RV,  Blanchard  JM,  Greenstreet  RL:  Breast  reconstruction  — Se- 
lection, timing  and  local  recurrence.  Ann  Plast  Surg  1983;10:265-269. 

5.  GBLUand  MD,  Larson  DL,  Copeland  EM:  Appropriate  timing  for  breast 
reconstruction.  Plast  Reconstr  Surg  1983;72:335-337. 

6.  Hartrampf  CR,  Scheflan  M,  Black  PW:  Breast  reconstruction  with  a trans- 
verse abdominal  island  flap.  Plast  Reconstr  Surg  1982;69:216-224. 

7.  Fugino  T,  Harshima  T,  Aoyad  F:  Reconstruction  for  aplasia  of  the  breast 
and  pectoral  region  by  microvascular  transfer  of  a free  flap  from  the 
buttock.  Plast  Reconstr  Surg  1975;56:178-181. 

8.  Shaw  WW:  Breast  reconstruction  by  superior  gluteal  microvascular  free 
flaps  without  silicone  implants.  Plast  Reconstr  Surg  1983;72:490-499. 


Drs  Lu  and  Swartz  are  from  the  Dept  of  Surgery,  Division  of  Plastic 
Surgery,  at  Tulane  Medical  School  in  New  Orleans. 

Reprints  will  not  be  available. 


JOURNAL  VOL  140  JUNE  45 


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SURGICAL  MANAGEMENT 
OF  IMPOTENCE: 

NEW  MODALITIES 


NEIL  BAUM,  MD 


Impotence  is  a common  problem  affecting  millions 
of  Amerian  men.  Of  these,  50%  are  impotent  on 
the  basis  of  physical  or  organic  causes.  This  article 
reviews  the  most  recent  advances  in  the  surgical 
management  of  impotence. 


Twenty  years  ago,  most  patients  with  impotence 
were  considered  to  have  psychogenic  or  emotional 
causes  for  their  sexual  dysfunction.  Following  the  pi- 
oneering work  of  Masters  and  Johnson  and  with  the 
assistance  of  new  diagnostic  techniques,  nearly  50% 
of  all  impotent  patients  have  been  found  to  have  an 
organic  or  physical  cause  of  their  erectile  dysfunction. 

In  the  past,  most  cases  of  organic  impotence  were 
treated  with  testosterone  injections  and  penile 
prostheses.  This  article  reviews  new  modalities  of  sur- 
gical management  of  impotence. 

VASCULOGENIC  IMPOTENCE 

Arterial  Insufficiency 

In  1923,  Leriche  recognized  the  relationship  between 
arterial  insufficiency  and  erectile  dysfunction.^  The 
clinical  syndrome  he  described  consisted  of  claudi- 
cation in  the  lower  extremities,  buttock  pain,  and  im- 
potence. The  pathology  consisted  of  occlusion  of  the 
distal  aorta  or  the  common  iliac  arteries.  Since  that 
initial  report,  very  little  had  been  done  in  treating 
vasculogenic  impotence  until  the  70s.  Now,  with  a 
better  imderstanding  of  vascular  pathophysiology  and  ► 

JOURNAL  VOL  140  JUNE  47 


new  diagnostic  tests  to  identify  vasculogenic  impo- 
tence, effective  treatment  for  this  common  cause  of 
impotence  is  on  the  horizon. 

The  arterial  blood  supply  to  the  penis  originates 
from  the  hypogastric  artery  and  the  internal  pudendal 
artery.  The  internal  pudendal  supplies  the  common 
penile  and  finally  the  dorsal  penile  and  the  cavernosal 
arteries.  With  appropriate  pelvic  nerve  stimulation, 
arteriolar  resistance  decreases  and  the  blood  supply 
to  the  corpora  cavernosa  subsequently  increases  with 
resulting  tumescence  and  rigidity.  With  occlusion  at 
either  the  proximal  or  distal  end  of  the  blood  supply, 
penis  erectile  dysfunction  can  occur.  Patients  with 
arterial  occlusive  disease  have  a history  of  progressive 
loss  of  tumescence  and  rigidity,  and  nocturnal  penile 
tumescence  testing  (NDT)  shows  decreased  or  absent 
nocturnal  erections. 

There  is  one  disorder  described  as  “pelvic  steal 
syndrome"  in  which  the  patient  can  obtain  an  erection 
but  fail  to  maintain  it  after  vaginal  penetration  and 
pelvic  thrusting.^  Patients  with  pelvic  steal  syndrome 
have  normal  NPT  tests  and  can  maintain  the  erection 
when  the  male  is  in  the  inferior  or  supine  position. 
The  arterial  occlusion  in  pelvic  steal  syndrome  occurs 
at  the  level  of  the  external  iliac  or  the  hypogastric 
artery.  These  patients  can  obtain  an  erection,  but  with 
physical  exertion,  the  blood  supply  is  subtracted  or 
"stolen"  from  the  erectile  bodies  and  diverted  to  the 
muscles  of  the  pelvis  and  lower  extremities  resulting 
in  detumescence. 

The  diagnostic  tests  for  vasculogenic  impotence 
begin  with  noninvasive  tests  such  as  the  Doppler  pe- 
nile blood  pressure  determination.  The  penile  blood 
pressure  is  indexed  against  the  brachial  artery  blood 
pressure.  A normal  penile-brachial  index  is  1.0  and 
an  index  <0.6  is  highly  suggestive  of  arterial  insuf- 
ficiency. If  the  history  and  the  Doppler  study  suggest 
arterial  insufficiency  and  the  patient  is  a candidate  for 
a revascularization  operation,  then  the  location  of  the 
occlusion  is  identified  by  selective  internal  pudendal 
angiography. 

Vascular  insufficiency  can  be  divided  into  two 
treatment  categories:  proximal  occlusive  disorders  and 
distal  occlusive  disorders. 

Proximal  disorders  involve  the  distal  aorta,  com- 
mon iliac  arteries,  or  the  hypogastric  arteries.  Man- 
agement of  proximal  occlusive  disorders  includes 
standard  graft  bypass  procedures,  endarterectomies, 

48  JOURNAL  VOL  140  JUNE 


Fig  1.  Dynamic  corpora  cavernosogram  demon- 
strating venous  leak  (arrow). 


and,  currently,  the  use  of  transluminal  balloon  an- 
gioplasties.^ 

Distal  occlusive  disorders  have  been  successfully 
treated  with  revascularization  procedures  using  op- 
tical magnification.  There  are  a variety  of  techniques 
to  accomplish  the  revascularization  of  the  distal  penile 
arterial  blood  supply.  Most  of  these  techniques  are 
based  on  either  1)  anastomosis  of  the  inferior  epigas- 
tric artery  directly  to  the  corpora  cavernosa  or  to  the 
deep  dorsal  vein  of  the  penis  and  then  creation  of  an 
anastomosis  between  the  arterialized  vein  and  the 
corpora  cavernosa,  or  2)  arterialization  of  the  patent 
distal  penile  arteries.  The  successful  results  of  these 
revascularization  procedures  vary  from  30%  to  80%.^ 
The  most  successful  results  occur  in  the  younger  pa- 
tient who  has  vasculogenic  impotence  on  the  basis  of 
pelvic  or  perineal  trauma. 

Venous  Incompetence 

Ligation  of  the  dorsal  vein  of  the  penis,  reported  at 
the  turn  of  the  century,  was  one  of  the  first  surgical 
approaches  in  the  treatment  of  impotence.^  This  pro- 
cedure did  not  meet  with  significant  success  and  was 
abandoned.  Recently,  the  importance  of  the  venous 


system  in  the  physiology  of  erection  has  become  ap- 
parent and  new  diagnostic  techniques  have  been  de- 
veloped to  identify  abnormal  venous  drainage  leading 
to  correction  of  abnormal  venous  drainage  from  the 
corpora  cavernosa. 

Studies  on  the  physiology  of  an  erection  have 
demonstrated  that  the  venous  outflow  from  the  cor- 
poral bodies  decreases  during  erection.  When  there 
is  a failure  to  decrease  this  venous  outflow  from  the 
erectile  bodies,  a "venous  leak"  situation  occurs  and 
there  will  be  failure  to  trap  the  blood  supply  in  the 
penis. ^ Patients  with  venous  leak  have  a history  of 
partial  erections,  lacking  the  rigidity  for  adequate  vag- 
inal penetration.  Often  the  patients  describe  "stuff- 
ing" the  partially  erect  penis  into  the  vagina.  Venous 
leak  impotence  is  one  of  the  few  physical  causes  of 
primary  erectile  dysfunction. 

The  diagnosis  of  venous  leak  impotence  is  made 
by  dynamic  corpora  cavemosography.^  This  tech- 
nique consists  of  infusion  of  contrast  material  into  the 
corpora  cavernosa  and  measurement  of  the  pressure 
within  the  corpora  cavernosa  together  with  simulta- 
neous fluoroscopic  monitoring,  when  tumescence  or 
erection  occurs.  The  criteria  for  venous  leak  by  this 
diagnostic  procedure  include:  1)  excessive  inflow  rates 
necessary  to  produce  an  erection,  2)  early  visualiza- 
tion and  dilatation  of  the  veins  draining  the  corpora 
cavernosa  (Fig  1),  and  3)  early  washout  of  the  contrast 
material  from  the  corpora  cavernosa. 

The  treatment  of  venous  leakage  consists  of  li- 
gation of  the  abnormally  draining  veins  and  their  trib- 
utaries. Nearly  50%  to  75%  of  the  patients  with  doc- 
umented venous  leak  will  have  improvement  in  their 
erections  following  surgical  ligation  of  the  abnormal 
veins.® 

PEYRONIE'S  DISEASE 

Peyronie's  disease  or  "bent  penis"  deformity  is  a com- 
mon cause  of  erectile  dysfunction.  The  etiology  of  the 
fibrosis  or  scar  formation  replacing  the  erectile  tissue 
within  the  corpora  cavernosa  is  unknown.  There  have 
been  numerous  conservative  approaches  to  this  prob- 
lem none  of  which  has  been  uniformly  successful.^  It 
is  difficult  to  assess  conservative  management  be- 
cause many  cases  of  Peyronie's  disease  undergo  spon- 
taneous remission.  The  indications  for  surgical  cor- 
rection of  Peyronie's  disease  include:  1)  persistent 
deformity  for  longer  than  one  year,  2)  significant  de- 


formity that  makes  vaginal  penetration  difficult  or 
painful  to  either  the  patient  or  his  partner,  and  3) 
painful  erections.  The  techniques  available  for  cor- 
rection of  Peyronie's  disease  include  plaque  excision 
and  replacement  with  either  a dermal  graft  or  a syn- 
thetic material  such  as  Dacron.  These  procedures  are 
used  if  there  is  minimal  replacement  of  the  erectile 
tissue  with  scar  formation  and  the  patient  is  potent. 

If  there  is  significant  replacement  of  the  erectile  tissue 
and  the  patient  is  impotent,  then  one  of  the  penile 
prostheses  is  inserted  after  removal  of  the  fibrous 
plaque. 

PENILE  PROSTHESES 

In  the  late  60s  the  first  serriirigid  rod  (SRR)  penile 
prosthesis  was  made  available  for  the  treatment  of 
impotence. This  prosthesis  was  effective  in  creating 
an  erection  adequate  for  vaginal  penetration.  How- 
ever, the  SRR  is  associated  with  a permanent  erection 
that  causes  problems  with  concealment  and  psycho- 
logical acceptance.  In  the  early  70s,  Dr  F.  Brantley 
Scott  developed  the  inflatable  multicomponent  penile 
prosthesis. This  device  consisted  of  two  inflatable 
cylinders  that  were  inserted  into  the  corporal  bodies, 
a pump  that  is  inserted  into  the  scrotum,  and  a res- 
ervoir placed  behind  the  pubic  symphysis.  This  pro- 
duces a natural-appearing  erection  that  increases  in 
both  girth  and  length  when  the  device  is  inflated  and 
a flaccid  penis  when  the  device  is  deflated.  As  a result, 
the  inflatable  perule  prosthesis  does  not  cause  prob- 
lems with  concealment  or  acceptance. 

As  in  most  areas  of  medicine,  new  technology 
has  resulted  in  improvements  in  the  devices  and  in 
simplification  of  surgical  procedures.  Currently,  there 
are  two  brands  of  self-contained  penile  prostheses: 
Flexi-Flate®  (Surgitek,  Racine,  Wis)  and  Hydro  Flex® 
(American  Medical  Systems,  Minnetonka,  Minn).  One, 
the  Hexi-Hate,  consists  of  two  hydraulic  cylinders  each 
containing  a reservoir  located  directly  behind  the  in- 
flate/deflate mechanism  (Fig  2). This  prosthesis  offers 
the  advantages  of  rigidity  and  flaccidity  but  with  less 
difficulty  in  implantation  than  the  multi-component 
inflatable  penile  prosthesis. 

A new  mechanical  device  has  been  developed 
that  does  not  use  the  hydraulic  principle  of  moving 
fluid  by  a pump  mechanism  between  a reservoir  and 
cylinders  within  the  corpora  cavernosa.  This  Omni- 
phase prosthesis  (Dacomed  Corp,  Minneapolis,  Minn)  ^ 

JOURNAL  VOL  140  JUNE  49 


Fig  2.  Self-contained  inflatable  penile  prosthesis  (photo  courtesy  of  Medical  Engineering  Corp,  Racine, 
Wis). 


>■ 

% 

/■ 

Fig  3.  Omniphase  prosthesis  (photo  courtesy  of  Dacomed  Corp,  Minneapolis,  Minn) 


consists  of  a mechanical  cable  which  is  attached  to  an 
activating  mechanism  within  the  prosthesis  (Fig  3). 
The  prosthesis  can  be  activated  by  bending  the  penis 
downward  toward  the  scrotum.  When  the  penis  is 
released,  the  device  becomes  rigid  and  adequate  for 
intercourse.  The  device  is  deactivated  by  repeating 
the  process  and  the  penis  becomes  flaccid. 

Soon  to  be  marketed  is  the  Girth,  Placidity,  Sim- 
plicity (GFS)  Prosthesis®  (Mentor,  Goleta,  Calif)  which 
will  provide  the  most  natural  erection  and  which  will 
also  be  easy  to  surgically  implant.  This  is  a two  com- 
ponent hydraulic  inflatable  prosthesis  consisting  of 
cylinders  inserted  into  the  corporal  bodies  of  the  penis 
and  a combination  pump-reservoir  component  that  is 
placed  dependency  within  the  scrotum.  This  device 
provides  the  rigidity  and  flaccidity  of  the  Scott  pros- 
thesis together  with  the  simplicity  of  insertion  as  the 
semirigid  rod  prosthesis, 

SUMMARY 

The  management  of  organic  impotence  has  developed 
dramatically  in  the  last  few  years.  It  is  possible  to 
accurately  diagnose  most  causes  of  impotence  and  to 
effectively  treat  almost  all  patients  with  this  common 
problem.  ■ 

REFERENCES 

1.  Leriche  R:  Des  obliterations  arterielles  hautes  comme  cause  d'une  in- 
suffisance  circulatoire  des  membres  inferiers.  Bull  Soc  Chirurgie 
1923;49(33):1404-1406. 


2.  Goldstein  1,  Siroky  MB,  Nath  RL,  et  al:  Vas- 
culogenic  impotence;  Role  of  the  pelvic  steal 
test.  / Urol  1982;128(2):300-306. 

3.  Goldwasser  B,  Carson  CC,  Braun  SD,  et  al.  Im- 
potence due  to  the  pelvic  steal  syndrome:  Treat- 
ment by  Uiac  transluminal  angioplasty.  / Urol 
1985;133(5):860-861. 

4.  Goldstein  1:  Arterial  revascularization  proce- 
dures. Semin  Urol  1986;4(4):252-258. 

5.  Wooten  JS:  Ligation  of  the  dorsal  vein  of  the 
penis  as  a cure  for  atonic  impotence.  Tex  Med 
1903;18(8):325-328. 

6.  Wagner  G:  Erection:  Physiology  and  endocri- 
nology, in  Impotence:  Physiological,  Psychological, 
Surgical  Diagnosis  and  Treatment,  Wagner  G, 
Green  R (eds).  New  York,  Plenum,  1981,  25-36. 

7.  Puyau  FA,  Lewis  RW:  Corpus  cavemosogra- 
phy:  Pressure,  flow  and  radiography.  Invest  Ra- 
diol 1983;18(6):517-522. 

8.  Lewis  RW,  Puyau  FA:  Procedures  for  decreas- 
ing venous  drainage.  Semin  Urol  1986;4(4):263- 
272. 

9.  Mira  JG:  Is  it  worthwhile  to  treat  Peyronie  dis- 
ease? Urology  1980;16(l):l-6. 

10.  Furlow  WL:  Therapy  of  impotence,  in  Clinical 
Neuro-Urology,  Krane  RJ,  Siroky  MB  (eds).  Bos- 
ton, Little  Brown  and  Co,  1979,  213-228. 

11.  Scott  FB,  Byrd  GI,  Karacan  I:  Erectile  impotence 
treated  with  an  inflatable  penile  prosthesis:  Five 
years  of  clinical  experience.  JAMA 
1979;241(24):2609-2612. 


Dr  Baum  is  a urologist  affiliated  with  Touro  Infirmary  in  New  Orleans. 

Reprint  requests  should  be  sent  to  Dr  Baum  at  3525  Prytania  St, 
Suite  614,  New  Orleans,  LA  70115. 


50  JOURNAL  VOL  140  JUNE 


REPORTING  AIDS  CASES  IN  LOUISIANA 


WHO  SHOULD  REPORT? 

Every  physician  is  required  by  law  to  report  any  case  or  suspected  case  of  AIDS  which  he  or  she  is  attending, 
has  examined,  or  has  prescribed  for  (Louisiana  Sanitary  Code,  Chapter  II,  §2:004). 


WHAT  SHOULD  BE  REPORTED? 

The  presence  of  a reliably  diagnosed  disease  at  least  moderately  indicative  of  an  underlying  cellular  immune 
deficiency,  with  no  other  known  underlying  cause  of  cellular  immune  deficiency  nor  any  other  cause  of  reduced 
resistance  reported  to  be  associated  with  that  disease.  This  involves  completion  of  a two-page  case  report 
form  (available  from  the  Epidemiology  Section  or  any  parish  health  unit)  to  determine  if  the  person  meets 
the  Centers  for  Disease  Control  AIDS  surveillance  case  definition. 


WHEN  SHOULD  I REPORT? 

The  report  should  be  made  promptly  at  the  time  the  physician  first  visits,  examines  or  prescribes  for  the 
patient  (Louisiana  Sanitary  Code,  Chapter  II,  §2:004). 


WHERE  SHOULD  I REPORT? 

A diagnosed  or  suspected  case  of  AIDS  should  be  reported  directly  to  the  Epidemiology  Section  in  New 
Orleans. 

By  phone:  (504)  568-5005 

By  mail:  La.  Office  of  Preventative  and  Public  Health  Services 
Epidemiology  Section 
PO  Box  60630 
Room  615 

New  Orleans,  LA  70160 


WHY  REPORT  AIDS  CASES? 

In  addition  to  being  required  by  law,  monitoring  the  distribution  and  characteristics  of  patients  with  AIDS 
is  the  only  method  currently  available  for  detecting  changes  in  the  epidemiology  of  Human  Immunodefi- 
ciency Virus  (HIV).  Knowledge  of  the  impact  of  HIV  on  Louisiana  residents  can  help  detect  new  or  unusual 
modes  of  transmission  and  assist  in  targeting  high  risk  groups  for  education  and  prevention  programs. 


CONFIDENTIALITY  CONCERNS 

All  reports  are  kept  absolutely  confidential.  Names  of  patients,  physicians  or  hospitals  are  not  released  under 
any  circumstances. 


JOURNAL  VOL  140  JUNE  53 


CALENDAR 

JL,  JBk  Jrnmmm  MLmm  «JL  ^1  WLmt!^  JIL,  «mL  JHw 


July 


July  1-5 

2nd  Annual  Family  Practice  Board  Review,  San  Diego.  Con- 
tact: Office  of  Continuing  Medical  Education,  UC  San  Diego  School 
of  Medicine,  M-017,  La  Jolla,  CA  92093;  (619)534-3940. 

July  6-13 

Breast  Imaging  and  Ultrasound,  Alaska  88:  Cruise  the  In- 
land Passage.  Contact:  Medical  Seminars  International  Inc,  21915 
Roscoe  Blvd,  Suite  222,  Canoga  Park,  CA  91304;  (818)719-7380. 

July  14-16 

4th  Annual  Berkshire  Medical  Conference:  Advances  in  Car- 
diology, Hancock,  Massachusetts.  Contact:  Berkshire  AHEC, 
(413)447-2417. 

July  16-18 

Laboratory  and  Clinical  Aspects  of  Microbiological 
Diagnosis,  Newport  Beach,  California.  Contact:  Sydney  M. 
Finegold,  MD,  Dept  of  Continuing  Education  in  Health  Sciences, 
Room  614,  UCLA  Extension,  10995  Le  Conte  Ave,  Los  Angeles, 
CA  90024;  (213)825-7257. 

July  17-22 

Physicians  and  Their  Families:  Balancing  Commitments  to 
Family  and  Profession,  Estes  Park,  Colorado.  Contact:  Jayne 
Roberts,  Conference  Coordinator,  Division  of  Continuing  Educa- 
tion, The  Menninger  Clinic,  Box  829,  Topeka,  KS  66601-0829; 
(800)288-7377. 

July  17-22 

13th  Annual  National  Wellness  Conference,  Stevens  Point, 
Wisconsin.  Contact:  National  Wellness  Institute,  South  Hall, 
University  of  Wisconsin,  Stevens  Point,  WI 54481;  (715)346-2172. 

July  19-23 

Louisiana  Academy  of  Family  Physicians  Annual  Scientific 
Assembly,  Sandestin  Beach  Hilton,  Destin,  Florida.  Contact: 
LAPP,  4705  Iberville  St,  New  Orleans,  LA  70119. 

July  21  - August  2 

Italy  and  the  Swiss  Alps,  Sponsored  by  INTRAV  and  the 
Louisiana  State  Medical  Society.  Contact:  Anita  Bums,  LSMS, 
1700  Josephine  St,  New  Orleans,  LA  70113;  (504)561-1033, 
(800)462-9508. 

July  24-28 

34th  Annual  Southern  OB-GYN  Seminar,  Asheville,  North 
Carolina.  Contact:  Dr.  George  Schneider,  Ochsner  Clinic,  Dept 

54  JOURNAL  VOL  140  JUNE 


of  OB-GYN,  1514  Jefferson  Hwy,  New  Orleans,  LA  70121; 
(504)838-4031. 

July  24-29 

8th  Annual  Internal  Medicine  Review,  Hilton  Resort,  South 
Padre  Island,  Texas.  Contact:  Scott  & White  Continuing  Medical 
Education  Office,  2401  South  31st  St,  Temple,  TX  76508; 
(817)774-2350. 

July  25-29 

Sports  Medicine  1988:  A Practical  Approach  to  Caring  for 
Today's  Athlete,  San  Diego.  Contact:  Office  of  Continuing 
Medical  Education,  UC  San  Diego  School  of  Medicine,  M-017,  Im 
Jolla,  CA  92093-0617;  (619)534-3940. 


August 


August  13-14 

Anesthesia  for  the  Cardiac  Patient  Having  Non-Cardiac 
Surgery,  San  Diego.  Contact:  American  Society  of  Anesthe- 
siologists, 515  Busse  Hwy,  Park  Ridge,  IL  60068. 

Discussions  of  Current  Hand  Care  Concepts,  San  Diego. 
Contact:  Plastic  Surgery  Educational  Foundation,  444  East  Algon- 
quin Rd,  Arlington  Heights,  IL  60005;  (312)228-9900. 

August  14-19 

Wilderness  Medicine,  Snowmass,  Colorado.  Contact:  Office 
of  Continuing  Medical  Education,  UC  San  Diego  School  of 
Medicine,  M-017,  La  Jolla,  CA  92093-0617;  (619)534-3940. 

August  21-30 

INTRAV  Cruise  on  the  Queen  Elizabeth  2 and  London,  Con- 
tact: Anita  Bums,  Louisiana  State  Medical  Society,  1700  Josephine 
St,  New  Orleans,  LA  70113;  (504)561-1033,  (800)462-9508. 

August  27 

Teleplast  Teleconference  on  Fasciocutaneous  Flaps, 

Metairie,  Shreveport,  and  Baton  Rouge,  Louisiana.  Contact: 
Plastic  Surgery  Educational  Foundation,  444  East  Algonquin  Rd, 
Arlington  Heights,  IL  60005;  (312)228-9900. 


I 


September 


September  6-9 

3rd  Annual  Plastic  Surgery  of  the  Breast  Symposium,  San- 
ta Fe,  New  Mexico.  Contact:  Plastic  Surgery  Educational  Foun- 
dation, 444  East  Algonquin  Rd,  Arlington  Heights,  IL  60005; 
(312)228-9900. 

September  10-18 

4th  Annual  Fall  Ultrasound  Symposia,  London  and  Paris. 
Contact:  Annual  Fall  Ultrasound  Meeting,  Medical  Seminars  In- 
ternational Inc,  21915  Roscoe  Blvd,  Suite  222,  Canoga  Park,  CA 
91304;  (818)719-7380. 

September  14-19 

Cosmetic  Surgery  of  the  Face  and  Breast,  Monte  Carlo, 
Monaco.  Contact:  Francine  Leinhardt,  Conference  Coordinator, 
210  East  64th  St,  New  York,  NY  10021;  (212)838-9200  ext  2776. 

September  17-18 

Metropolitan  Regional  Refresher  Course,  Las  Vegas.  Con- 
tact: American  Society  of  Anesthesiologists,  515  Busse  Hwy,  Park 
Ridge,  IL  60068. 

September  17-19 

4th  Aimual  Meeting  of  the  American  Society  for  Reconstruc- 
tive Microsurgery,  Baltimore.  Contact:  ASRM,  3025  South 
Parker  Rd,  Suite  65,  Aurora,  CA  80014. 


October 


October  3-5 

NIH  Consensus  Development  Conference:  Urinary  Incon- 
tinence in  Adults,  Bethesda,  Maryland.  Contact:  Conference 
Registrar,  Prospect  Associates,  Suite  500,  1801  Rockville  Pike, 
Rockville,  MD  20852;  (30D468-MEET. 

October  3-7 

6th  Annual  Comprehensive  Review  of  Vascular  Surgery, 

Santa  Monica,  C^ornia.  Contact:  UCLA  Extension,  PO  Box 
24901,  Los  Angeles,  CA  90024-0901;  (213)825-1901. 

October  8-12 

American  Society  of  Anesthesiologists  Annual  Meeting,  San 

Francisco.  Contact:  ASA,  515  Busse  Hwy,  Park  Ridge,  IL  60068. 


October  8-15 

10th  International  Seminar  on  Operative  Arthroscopy, 

Kauai,  Hawaii.  Contact:  UCLA  Extension,  Dept  of  Continuing 
Education,  PO  Box  24901,  Los  Angeles,  CA  90024-0901; 
(213)825-1901. 

October  8-16 

13th  Aimual  International  Body  Imaging  Conference,  Maui, 
Hawaii.  Contact:  Annual  Body  Imaging  Conference,  21915  Roscoe 
Blvd,  Suite  222,  Canoga  Park,  CA  91304;  (818)700-9821. 

October  12-14 

Hip  and  Knee  Reconstructive  Surgery  1988,  Kauai,  Hawaii. 
Contact:  UCLA  Extension,  Health  Sciences  Dept,  PO  Box  24901, 
Los  Angeles,  CA  90024-0901;  (213)825-1901. 

November 


November  2-5 

Optimizing  Management  of  Primary  Bone  Tumors:  An  In- 
ternational Symposium  Emphasizing  the  Multidisciplinary 
Approach,  Houston.  Office  of  Conference  Services,  M.  D.  Ander- 
son Cancer  Center,  1515  Holcombe  Blvd,  Houston,  TX  77030; 
(713)792-2222. 

November  5 

Teleplast  Teleconference  on  Management  of  Craniomax- 
illofacial  Trauma,  Metairie,  Shreveport,  Baton  Rouge,  Louis- 
iana. Contact:  Plastic  Surgery  Educational  Foundation,  444  East 
Algonquin  Rd,  Arlington  Heights,  IL  60005;  (312)228-9900. 

November  10-13 

Lasers  for  the  Plastic  Surgeon,  Orlando,  Florida.  Contact: 
Plastic  Surgery  Educational  Foundation,  444  East  Algonquin  Rd, 
Arlington,  Heights,  IL  60005;  (312)228-9900. 

November  11-12 

Advances  in  the  Treatment  of  Pediatric  Bones:  Craniofacial, 
Orthopedic,  Neurosurgical,  Dallas.  Contact:  Linda  Henry, 
Humana  Hospital  - Medical  City  Dallas,  7777  Forest  Lane,  Dallas, 
TX  75230;  (214)661-7000. 

November  17-20 

Assuring  the  Future  Fiscal  Survival  of  Consultation  — 
Liaison  Psychiatry  and  Psychosomatic  Medicine,  New 

Orleans.  Contact:  Academy  of  Psychosomatic  Medicine,  5824  N 
Magnolia,  Chicago,  IL  60660;  (312)784-2025. 


JOURNAL  VOL  140  JUNE  55 


PROFESSIONAL  LISTINGS 


THE  FERTILITY  INSTITUTE  OF  NEW  ORLEANS 


(A  Professional  Corporation) 


Richard  P.  Dickey,  MD,  PhD 

Diplomate,  American  Board  of 
Reproductive  Medicine 
Diplomate,  American  Board  of 
Obstetrics  and  Gynecology 


Steven  N.  Taylor,  MD 

Diplomate,  American  Board  of 
Obstetrics  and  Gynecology 


1 


David  N.  Curole,  MD  Phillip  H.  Rye,  MD 

Diplomate,  American  Board  Diplomate,  American  Board 

of  Obstetrics  and  Gynecology  of  Obstetrics  and  Gynecology 


Terry  Olar,  PhD 

Director,  InVitro  Laboratory 
Member,  Society  for  the 
Study  of  Reproduction 


REFERRALS  ACCEPTED  FOR  IN  VITRO  FERTILIZATION 
AND  OTHER  INFERTILITY  THERAPY  INCLUDING; 

MICROSURGERY  AND  LASER-MICROSURGERY  OF  THE  INFERTILE  FEMALE 
MANAGEMENT  OF  RECURRENT  AND  THREATENED  ABORTIONS  THROUGH  THE  FIRST  TRIMESTER 
LABORATORY  FACILITIES  FOR  COMPLETE  ANDROLOGY  AND  ENDOCRINOLOGY  TESTING 
INCLUDING  OVUM  PENETRATION  (HAMSTER  EGG) 


MAIN  OFFICE 

SLIDELL  OFFICE 

UPTOWN  OFFICE 

6020  Bullard  Ave 
New  Orleans,  LA  70128 
(504)  246-8971 
(504)  246-8795 

700  Cause  Blvd 
Suite  101 
SlideU,  LA  70458 

2633  Napoleon  Ave 
Suite  805 

New  Orleans,  LA  70115 

TOURO  INFIRMARY'S  CENTER  FOR  CHRONIC  PAIN 

AND 

DISABILITY  REHABILITATION 

1401  Foucher  St 
New  Orleans,  LA  70115 
(504)  897-8404 

Richard  H.  Morse,  MD 

Medical  Director 

Jackie  Chauvet 

Liaison  Coordinator 

Elizabeth  Messina,  RN 

Unit  Supervisor 

56  JOURNAL  VOL  140  JUNE 


JOURNAL 

OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY  July  1988 


STACKS 


- ^ 

The  five  horsemen  of  rheumatology 


ALSO 


KAWASAKI'S  SYNDROME  ACCOMPANIED 
BY  BONE  MARROW  SUPPRESSION 


CESAREAN  CHILDBIRTH  RATE  AMONG 
WOMEN  IN  THE  NEW  ORLEANS  AREA 


.rc  C^^^ 


VJ^ 


Louisiana 


Physicians 


Insurance  Agency,  INC. 

A VVhollv  Owned  Subsidiars'  of  LAMMICO 


SPECIALLY  PRICED  PRODUCTS  OFFERED: 

• Exclusive  Physicians  Office  Package 

• Dividend  Potential 


• Disability  Income  Protection 

• YOU  define  YOUR  medical  specialty  under  definition  of 
disability 

• Additional  15%  annual  discount  to  LAMMICO  insureds 

• Prestige  Homeowners  Program 

• Personal  Umbrella 


• 433  Metairie  Road,  Suite  602  • 

• Metairie,  Louisiana  70005  • 

• (504)  837-3257  • 1-800-331-5777  • 

A COMMITMENT  TO  SERVE  THE  LOUISIANA  PHYSICIAN 


EDITOR 


CONWAY  S.  MAGEE,  MD 

CHIEF  EXECUTIVE  OFFICER 

DAVE  TARVER 

GENERAL  MANAGER 

RENE  ABADBE 

MANAGING  EDITOR 

BONNIE  L.  BLUNDELL 

ADVERTISING  SALES 

CHARLOTTE  SPOONER 

JOURNAL  COMMITTEE 

Chairman,  CONWAY  S.  MAGEE,  MD 
A.G.  KLEINSCHMIDT  JR,  MD 
PAUL  F.  LARSON,  MD 
W.  CHARLES  MILLER,  MD 
EMILE  K.  VENTRE  JR,  MD 
Ex  officio,  DANIEL  H.  JOHNSON  JR,  MD 

EDITORIAL  BOARD 

KENNETH  B.  FARRIS,  MD 
RODNEY  C.  JUNG,  MD 
CONWAY  S.  MAGEE,  MD 
W.  CHARLES  MILLER,  MD 
ELI  SORROW,  MD 
CLAY  A.  WAGGENSPACK  JR,  MD 
WINSTON  H.  WEESE,  MD 
PATRICK  W.  PEAVY,  MD 

EXECUTIVE  COMMITTEE 

DANIEL  H.  JOHNSON  JR,  MD 
MILTON  C.  CHAPMAN,  MD 
JOHN  C.  COOKSEY,  MD 
JAMES  W.  VILDIBILL  JR,  MD 
SAMUEL  A.  LEONARD,  MD 
R.  BRUCE  WILLIAMS,  MD 
HOWARD  A.  NELSON  JR,  MD 
RONALD  J.  FRENCH,  MD 
FRANK  J.  GEORGE,  MD 
PHILIP  A.  ROBICHAUX  JR,  MD 
JAMES  R.  BERGERON,  MD 
DAVID  M.  WALSWORTH,  MD 
CHARLES  D.  BELLE AU,  MD 
G.  MICHAEL  KENT,  MD 
LEO  L.  LOWENTRITT  JR,  MD 
EMILE  K.  VENTRE  JR,  MD 
STANFORD  A.  OWEN,  MD 
WALLACE  H.  DUNLAP,  MD 


Established  1844.  Owned  and  edited  by  The 
Journal  of  the  Louisiana  State  Medical  Society,  Inc, 
1700  Josephine  St,  New  Orleans,  LA  70113. 

Copyright  1988  by  The  Journal  of  the  Louisiana 
State  Medical  Society,  Inc 

Subscription  price  is  $12  per  year  in  advance, 
postage  paid  for  the  United  States;  $15  per  year  for 
all  foreign  countries  belonging  to  the  Postal  Union; 

$1.50  per  single  issue. 

Advertising:  Contact  Charlotte  Spooner,  1700 
Josephine  St,  New  Orleans,  LA  70113; 
(504)  561-1033,  (800)  462-9508. 

Postmaster:  Send  address  changes  to  1700 
Josephine  St,  New  Orleans,  LA  70113. 

The  JOURNAL  (ISSN  0024-6921)  is  published 
monthly  at  1700  Josephine  St,  New  Orleans,  LA 
70113.  Second-class  postage  paid  at  New  Orleans 
and  additional  mailing  offices. 

Articles  and  advertisements  published  in  the 
lOURNAL  are  for  the  interests  of  its  readers  and  do 
not  represent  the  official  position  or  endorsement 
of  The  Journal  of  the  Louisiana  State  Medical  Society, 
Inc  or  the  Louisiana  State  Medical  Society.  The 
JOURNAL  reserves  the  right  to  make  the  final 
decision  on  all  content  and  advertisements. 


JOURNAL 


""  OF  THE  LOUISIANA  STATE  MEDICAL  SOCIETY 

1988 

VOLUME  140  / NUMBER  7 / 

JULY 

ARTICLES 

Jack  Waxman,  MD 

24 

The  five  horsemen  of 
rheumatology 

Irwin  Cohen,  MD 
Michael  Whistler,  MD 

31 

Kawasaki's  syndrome 
accompanied  by  bone 
marrow  suppression 

Joan  H.  Wightkin,  MPH 
Linda  M.  Lambert,  MPH 

39 

Cesarean  childbirth  rate 
among  women  in  the 
New  Orleans  area 

DEPARTMENTS 


2 

Information  for  Authors 

3 

Viewpoint 

7 

ECG  of  the  Month 

9 

Books  Received 

11 

Otolaryngology/Head 
& Neck  Surgery  Report 

19 

Auxiliary  Report 

48 

" Calendar 

53 

Classified  Advertising 

Cover  illustration  by  Eugene  New,  New  Orleans 


INFORMATION  FOR  AUTHORS 


The  JOURNAL  of  the  Louisiana  State  Medical  Society  is  intended  to 
provide  pract/ca/ scientific  information  of  interest  to  a broad  spectrum 
of  physician  members  of  the  LSMS  and  to  meet  the  need  of  each  physi- 
cian to  maintain  a general  awareness  of  progress  and  change  in  clinical 
medicine.  The  content  is  designed  to  aid  the  practicing  physician  in 
giving  comprehensive  care  and  in  recognizing  the  need  for  special- 
ized treatment. 

The  JOURNAL  welcomes  material  for  publication  if  submitted  by  a 
Louisiana  physician  in  accordance  with  the  following  guidelines.  Ad- 
dress all  correspondence  to  the  Editor,  Journal  of  the  Louisiana  State 
Medical  Society,  1 700  Josephine  Street,  New  Orleans,  LA  701 1 3.  Con- 
tact the  managing  editor  with  any  questions  concerning  these  guidelines 
or  for  a checklist  to  assist  in  manuscript  preparation. 

MANUSCRIPTS  should  be  of  an  appropriate  length  due  to  the  policy 
of  the  JOURNAL  to  feature  concise  but  complete  articles.  (Some  sub- 
jects may  necessitate  exception  to  this  policy  and  will  be  reviewed 
and  published  at  the  Editor's  discretion.)  The  language  and  vocabulary 
of  the  manuscript  should  be  understandable  and  not  beyond  the  com- 
prehension of  the  general  readership  of  the  journal.  The  journal 
attempts  to  avoid  the  use  of  medical  jargon  and  abbreviations.  All  ab- 
breviations, especially  of  laboratory  and  diagnostic  procedures,  must 
be  identified  in  the  text.  Manuscripts  must  be  typed,  double-spaced 
with  adequate  margins.  (This  applies  to  all  manuscript  elements  in- 
cluding text,  references,  legends,  footnotes,  etc.)  The  original  and  one 
duplicate  should  be  submitted.  Pages  should  be  numbered.  An  ac- 
companying cover  letter  should  designate  one  author  as  correspon- 
dent and  include  his/her  address  and  telephone  number.  Manuscripts 
are  received  with  the  explicit  understanding  that  they  have  not  been 
previously  published  and  are  not  under  consideration  by  any  other 
publication.  Manuscripts  are  subject  to  editorial  revisions  as  deemed 
necessary  by  the  editors  and  to  such  modifications  as  to  bring  them 
into  conformity  with  journal  style.  The  authors  clearly  bear  the  full 
responsibility  for  all  statements  made  and  the  veracity  of  the  work 
reported  therein. 

REVIEWING  PROCESS.  Each  manuscript  is  reviewed  by  the  Editor 
and  by  a member(s)  of  the  Editorial  Board  or  the  Panel  of  Consultants 
from  whom  knowledgeable  opinions  are  sought.  The  acceptability  of 
a manuscript  is  determined  by  such  factors  as  the  quality  of  the 
manuscript,  perceived  interest  to  journal  readers,  usefulness  or  im- 
portance to  physicians,  and  the  current  backlog  of  accepted 
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descriptive.  (Avoid  telling  what  "will  be  described"  and  instead 
describe  it.)  The  abstract  should  be  intelligible  when  divorced  from 
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lOURNALS 

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use  during  surgery.  Am  ] Clin  Pathol  1979;71:680-692. 

BOOKS 

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tion in  Cardiovascular  Medicine,  ed  2,  Smith  )T  (ed).  New 
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ASSISTANCE  WITH  YOUR  ELDERLY  PATIENT  LOAD: 

CASE  EXAMPLE 


IT  WILL  COME  as  no  surprise  to  the 
I practicing  physician  that  a 
[growing  percentage  of  the  patient 
load  is  elderly.  The  increasing  age 
of  the  patient  load  brings  with  it  a 
set  of  problems  that  did  not  exist 
when  the  physician  was  in  train- 
ling.  Health  care  needs  of  the  el- 
derly population  are  changing: 
acute  care  needs  no  longer  domi- 
nate; chronic  diseases  account  for 
the  top  ten  disease  states  in  the  el- 
derly population.^ 

These  chronic  disease  states 
require  more  than  just  medical  in- 
tervention. Due  to  the  long  term 
course  of  treatment,  they  necessi- 
tate involving  community  re- 
sources and  family  counseling.  The 
treatment  is  not  only  for  the  dis- 
ease but  also  for  the  ongoing  con- 
sequences of  the  disease.^ 


CASE  REPORT 

A 66-year-old  white  woman  was 
brought  to  the  Louisiana  Geriatric 
Assessment  Center  by  her  son, 
who  wanted  to  have  his  mother  in- 
terdicted with  himself  as  curator, 
due  to  her  long  term  alcohol  and 
drug  abuse.  The  son  had  legal 
guardianship  in  Florida  but  was 
moving  his  mother  to  be  near  him 
in  Louisiana.  The  patient  had  a di- 
agnosis of  dementia  secondary  to 


her  alcohol  abuse.  She  had  re- 
ceived psychotherapy  and  halo- 
peridol  (Haldol®)  in  Florida  with 
no  improvement.  She  had  had  an 
oophorectomy  in  the  distant  past 
for  an  unknown  cause.  There  were 
no  known  allergies.  Medications  at 
time  of  visit  included  Haldol®  5 
mg  three  times  daily  and  benztro- 
pin  mesylate  (Cojentin®)  5 mg 
twice  a day. 

The  patient  had  also  been 
evaluated  by  the  Minnesota  Mul- 
tiphasic  Personality  Inventory  In- 
terpretive System  and  had  been  di- 
agnosed as  having  had  a psychotic 
episode.  She  had  some  alteration 
in  thought  processes  with  regard 
to  auditory  hallucinations  and  de- 
lusional thinking  for  which  she  had 
received  treatment  in  Florida. 

While  in  Florida,  she  had  lived 
alone.  Her  closest  relatives  were  in 
Louisiana.  Family  and  social  his- 
tories were  not  remarkable. 

On  examination,  the  patient 
was  pleasant  and  appeared  in  no 
distress.  Physical  findings  were 
unremarkable  except  for  the  men- 
tal status  examination  that  re- 
vealed a decrease  in  overall  mem- 
ory, especially  in  short-term 
memory.  The  psychosocial  inter- 
view revealed  a woman  who 
wanted  to  return  to  Florida  and 
who  very  much  wanted  to  main- 


tain her  independence  and  was 
fearful  of  nursing  home  place- 
ment. She  engaged  in  a variety  of 
activities,  including  shopping. 

The  diagnosis  after  the  initial 
assessment  agreed  that  she  had 
significant  cognitive  impairments. 
The  care  plan's  recommendations 
were:  to  continue  the  present  med- 
ications, to  immediately  stop  al- 
cohol consumption,  to  seek  a shel- 
tered living  environment  with 
supportive  services  and  supervi- 
sion, to  engage  in  community  ac- 
tivities such  as  senior  center  activ- 
ities, and  to  maintain  the  same  legal 
supervision  that  existed  in  Florida. 
Care  management  services  were 
suggested  to  ease  the  implemen- 
tation of  these  recommendations. 
The  patient  and  the  family  were 
encouraged  to  monitor  progress 
after  the  move  and  to  consider 
reassessment,  possibly  a reversal 
of  the  curatorship/guardianship,  if 
her  functioning  improved  with 
treatment. 

Six  months  later,  the  son 
phoned  requesting  a reassessment 
of  his  mother.  He  thought  that  she 
was  doing  much  better  and  wanted 
another  opinion  regarding  her 
functioning  capacity.  Upon  reas- 
sessment, it  was  found  that  she  was 
significantly  improved,  exhibited 
no  cognitive  deficits,  and  had  re-  k 


JOURNAL  VOL  140  JULY  3 


I 

1 


mained  off  alcohol.  The  patient  and 
her  family  had  followed  the  care 
plan  with  assistance  of  a care  man- 
ager. As  a result  of  these  findings, 
her  son  decided  to  have  the  in- 
terdiction reversed.  His  mother  was 
once  again  in  full  control  of  her  life 
legally  as  well  as  functionally. 

DISCUSSION 

The  American  College  of  Physi- 
cians recently  issued  a position  pa- 
per on  the  use  of  comprehensive 
functional  assessment  for  elderly 
patients.  In  summary  they  felt  that 
"functional  assessment  proce- 
dures should  be  recognized  as 
identifiable,  specific  cognitive 
services  . . . that  can  be  useful  in 
systematically  assessing  functional 
deficits  that  otherwise  might  be 
overlooked  by  conventional  ex- 
amination methods."  The  paper 
goes  on  to  say  that  clinical  practice 
should  include  the  provision  of  "a 
needed  measure  of  functional  out- 
come, by  comparing  changes  in 
function  over  time  as  affected  by 
disease  and  other  life  events  (such 
as  bereavement),  and  the  subse- 
quent management  of  these  prob- 
lems."^ 

In  the  above  case  the  diagnosis 
was  easy  and  had  already  been 
made.  What  had  been  missing  in 
the  evaluation  was  a frank  discus- 
sion of  the  long  term  consequences 
of  the  disease.  As  so  often  happens 
with  the  elderly,  it  is  the  manage- 
ment of  these  long  term  conse- 
quences that  is  the  most  trouble- 
some and  costly.  This  case 
demonstrates  that  careful  assess- 
ment and  care  planning  which  fo- 
cus on  diagnosis  and  its  long-term 
social,  financial,  and  psychological 
effects  can  benefit  the  patient  and. 


in  the  long  run,  save  dollars.  The 
dollars  Medicare  provided  for  the 
assessment  were  minimal  com- 
pared to  the  cost  of  long-term  in- 
stitutionalization . 

These  patients  do  need  a pri- 
mary care  physician,  but  many 
times  this  physician  is  called  upon 
not  only  to  make  medical  diag- 
noses and  prescribe  treatment  but 
to  make  legal  decisions  and  to  be 
an  information  and  referral  center 
for  all  supportive  community  serv- 
ices. 

The  geriatric  functional  as- 
sessment provides  all  of  the  above 
on  a consultative  basis.  The  as- 
sessment does  not  replace  the  pri- 
mary physician  but  rather  supplies 
a team  which  assesses  the  patient's 
physical  needs  in  the  broader  con- 
text of  environment,  family  dy- 
namics, and  past  social  history.  A 
care  plan  is  developed  which  de- 
scribes both  short-term  and  long- 
term goals  and  includes  commu- 
nity resources,  changes  in  living 
arrangements,  and  other  pertinent 
information.  This  plan  gives  the 
primary  physician  and  the  patient 
a blue  print  for  continued  treat- 
ment and  guidance. 

A related  and  supplementary 
service  is  care  management.  In  the 
case  of  this  patient,  a care  manager 
stepped  in  and  arranged  the  nec- 
essary services:  helping  her  with 
housing  decisions,  facilitating  her 
participation  in  senior  center  activ- 
ities, and  monitoring  her  compli- 
ance with  the  treatment  regime. 
Her  family  was  free  to  enjoy  her 
presence  and  to  continue  the  fi- 
nancial management.  They  were 
relieved  of  the  burden  of  single- 
handedly  trying  to  implement  the 
care  plan  and  of  negotiating  the  red 
tape  of  the  community  service  de- 


livery system.  The  physician  was 
free  to  continue  with  ongoing 
treatment  as  necessary  without 
being  expected  to  "fix"  her  world 
and  address  her  family's  concerns. 

Taken  together,  the  geriatric 
functional  assessment  process  and 
care  management  offer  a complete 
package  of  services  to  augment  the 
treatment  a physician  can  offer. 
They  are  commplementary  serv- 
ices to  support  medical  care  and 
manage  the  chronic  conditions  so 
prevalent  among  the  elderly  pop- 
ulation. ■ 

REFERENCES 

1.  Aging  America:  Trends  and  Projections.  US  Dept 
of  Health  and  Human  Services,  1985-86.  US 
Senate  Special  Committee  on  Aging,  American 
Association  of  Retired  Persons,  Federal  Coun- 
cil on  Aging,  Administration  on  Aging. 

2.  Rubenstein  LZ,  Campbell  LJ,  Kane  RL:  Clinics 
In  Geriatric  Medicine:  Geriatric  Assessment,  Vol 
3(1).  Philadelphia,  WB  Saunders  Co,  1987. 

3.  Comprehensive  Functional  Assessment  For  Elderly 
Patients.  American  College  of  Physicians,  Jan- 
uary 15,  1988. 


TIMOTHY  J.  HOLT,  MD 
SARA  S.  HUNT,  MSW 
MADELINE  MONROE,  RN 
ROSE  COLLEY,  MSW 


4 JOURNAL  VOL  140  JULY 


ECG  OF  THE  MONTH 


CAREFUL  NEGLECT 

JORGE  I.  MARTINEZ-LOPEZ,  MD 


The  tracing  shown  below  belongs  to  a 71-year-old  man  hospitalized  with  acute  onset  of  severe 
retrosternal  chest  pain.  The  continuous  rhythm  strip  was  recorded  before  therapy  was  begun. 


What  is  your  diagnosis?  Elucidation  is  on  page  8. 


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JOURNAL  VOL  140  JULY  7 


ECG  of  the  Month. 

Case  presentation  is  on  page  7. 

DIAGNOSIS  — Acute  inferior  wall  myocardial  infarction 
and  intermittent  bundle  branch  block 

Sinus  tachycardia,  at  a rate  of  107  times  a minute,  is 
present. 

The  interesting  feature  on  the  rhythm  strip  is 
that,  although  sinus  rhythm  is  present  throughout  its 
length,  there  are  two  different  QRS  morphologies. 
These  morphologies  and  their  responsible  mechan- 
isms are  the  subject  of  the  discussion  to  follow. 

DISCUSSION 

Two  types  of  QRS  complexes  are  identified  on  the 
rhythm  strip:  a QRS  complex  of  normal  duration;  a 
wide  QRS  complex  with  a duration  of  0.12  sec. 

To  facilitate  analysis  of  the  rhythm  strip,  let  us 
first  examine  the  narrow  QRS  complexes.  They  meas- 
ure 0.08  sec  in  duration  and  are  preceded  by  sinus  P 
waves  with  normal  PR  intervals.  These  findings  in- 
dicate that  the  narrow  QRS  complexes  occur  in  re- 
sponse to  the  prevailing  sinus  rhythm  and  that  con- 
duction into  the  ventricles  is  normal.  Prominent  in 
the  narrow  QRS  complexes  are  Q waves  and  elevated 
ST  segments  that  are  consistent  with  the  ECG  diag- 
nosis of  acute  inferior  wall  myocardial  infarction.  Acute 
inferior  wall  myocardial  infarction  is  most  often  the 
result  of  compromised  circulation  in  the  right  coro- 
nary artery;  less  often,  the  left  circumflex  coronary 
artery  is  the  vessel  involved.  In  either  case,  the  most 
common  conduction  abnormality  is  at  the  AV  junc- 
tional level  beause  the  AV  nodal  artery  comes  off  the 
vessel  irrigating  the  inferior  wall  of  the  left  ventricle. 

Let  us  now  turn  our  attention  to  the  wide  QRS 
complexes.  The  sequence  that  begins  after  the  fourth 
narrow  QRS  on  the  top  panel  starts  and  ends  with  a 
wide  QRS  that  is  premature,  relative  to  the  preceding 
cycle,  and  does  not  have  a sinus  P in  front  of  it.  The 
intervening  wide  QRS  complexes  of  that  sequence 
recur  regularly  and  are  preceded  by  sinus  Ps.  Towards 
the  end  of  the  third  panel,  a brief  sequence  of  wide 
QRS  complexes  starts  and  ends  abruptly,  without  a 
premature  wide  QRS.  Lastly,  in  the  bottom  panel,  the 
three-beat  wide  QRS  sequence  with  Ps  in  front  end 
with  a fourth  wide  QRS  that  is  premature.  Five  nar- 
row QRS  complexes  later,  a premature  wide  QRS  oc- 


curs alone. 

The  train  of  events  described  above  raise  ques- 
tions relative  to  the  mechanisms  responsible  for  the 
wide  QRS  complexes.  Do  they  present  supraventric- 
ular premature  complexes  conducted  downgrade  with 
aberration,  accelerated  idioventricular  rhythm,  or  in- 
termittent bundle  branch  block? 

The  possibility  that  all  of  the  wide  QRS  complexes 
represent  aberrant  ventricular  conduction  of  prema- 
ture supraventricular  impulses  can  be  dismissed 
quickly.  Although  premature  wide  QRS  complexes 
are  recorded  at  the  beginning  and  end  of  one  se- 
quence, at  the  end  of  another,  and  as  an  isolated  event 
(bottom  panel),  it  is  clear  that  all  the  other  wide  QRS 
complexes  are  preceded  by  sinus  Ps  with  a fixed  PR 
interval. 

Similarly,  accelerated  idioventricular  rhythm 
(AIVR)  is  an  unlikely  mechanism  responsible  for  the 
wide  QRS  complexes.  AIVR,  a relatively  common  ar- 
rhythmia in  acute  myocardial  infarction,  is  a ventric- 
ular escape  rhythm.  Therefore,  its  emergence  is 
marked  by  slowing  of  the  sinus  rhythm,  with  and 
without  intervening  “fusion  beats."  Because  AIVR  is 
an  escape  rhythm,  AV  dissociation  by  default  is  also  i 
present.  In  the  tracing  shown  here,  sinus  Ps  have  a 
constant  relationship  with  the  wide  QRS  complexes 
that  follow  them. 

The  third  option,  intermittent  bundle  branch 
block,  is  the  most  plausible.  The  majority  of  instances 
of  intermittent  bundle  branch  block  are  due  to  changes 
in  cycle  length  — even  when  minimal.  This  electro- 
physiological  phenomenon  is  termed  rate-related  or 
rate-dependent  bundle  branch  block.  In  such  cases,  ap- 
pearance of  the  bundle  branch  block  patterns  may 
occur  when  the  cardiac  cycle  length  either  narrows 
(tachycardia-dependent  block)  or  lengthens  (brady- 
cardia-dependent block).  On  occasion,  tachycardia- 
and  bradycardia-dependent  block  coexist. 

The  mechanisms  responsible  for  the  develop-  i 
ment  of  rate-dependent  block  have  yet  to  be  clarified. 

It  has  been  postulated  that  in  tachycardia-dependent 
block,  repolarization  is  prolonged,  whereas  the  bra- 
dycardia-dependent block  is  related  to  hypopolari- 
zation  and  reduction  in  membrane  responsiveness. 
Similar  mechanisms  have  been  proposed  for  rate-de-  ! 
pendent  blocks  observed  in  myocardial  ischemia.  As 
myocardial  ischemia  becomes  less,  intraventricular 
conduction  improves. 

In  the  present  case,  the  evolving  myocardial  in- 


8 JOURNAL  VOL  140  JULY 


I 

1, 


farction  played  a major  role  in  predisposing  the  pa- 
tient to  rate-dependent  block.  The  phenomenon  was 
transient  and  disappeared  after  the  myocardial  in- 
farction was  completed.  During  evolution  of  the  my- 
ocardial infarction,  minimal  lengthening  of  the  PP  in- 
terval appeared  to  be  responsible  for  the  rate- 
dependent  block  when  it  appeared  abruptly.  Minimal 
changes  in  cycle  length  may  not  be  clearly  obvious 
when  tracings  are  recorded  at  the  conventional  speed 
(25mm/sec),  but  may  become  obvious  at  a paper  speed 
of  lOOmm/sec.  In  other  portions  of  the  tracing,  supra- 
ventricular premature  impulses  conducted  aberrantly 
into  the  ventricles  set  the  stage  for  initiation  and/or 
termination  of  the  rate-dependent  block.  In  the  bot- 
tom panel,  however,  the  isolated,  premature  supra- 
ventricular impulse  conducted  with  aberration  failed 
to  trigger  what  others  did. 

Rate-dependent  block,  in  itself,  is  benign,  and 
does  not  require  medical  or  electrical  therapy,  only 
"careful  neglect."  In  other  words,  while  ECG  moni- 
toring and  awareness  of  the  presence  of  rate-depend- 
ent block  are  important,  intervention  is  not  necessary. 
Bradycardia-dependent  bilateral  bundle  branch  block 
deserves  special  attention,  as  it  may  result  in  parox- 
ysmal AV  block  and  hemodynamic  alterations. 

A final  word.  In  this  patient,  the  development  of 
the  bundle  branch  block  pattern  masked  the  ECG 
findings  of  acute,  evolving,  inferior  wall  myocardial 
infarction.  ■ 

SELECTED  REFERENCES 

1.  El-Sherif  N:  Tachycardia-dependent  versus  bradycardia-dependent  inter- 
mittent bundle  branch  block.  Br  Heart  J 1972;34:167-176. 

2.  Rosenbaum  MG,  Elizari  MV,  et  al:  The  mechanism  of  intermittent  bundle 
branch  block.  Relationship  to  prolonged  recovery,  hypopolarization  and 
spontaneous  diastolic  depolarization.  Chest  1973;63:666-667. 

3.  El-Sherif  N:  Tachycardia-  and  bradycardia-dependent  bimdle  branch  block 
after  acute  myocardial  ischemia.  Br  Heart  J 1974;36:291-301. 

4.  El-Sherif  N,  Scherlag  BJ,  Lazzara  R:  Bradycardia-dependent  conduction 
disorders.  J Electrocardiol  1976;9:1-4. 

5.  Mitamura  H,  Ogawa  S,  et  al:  A case  of  coexisting  tachycardia-  and  bra- 
dycardia-dependent bilateral  bundle  branch  block.  / Electrocardiol 
1981;14:195-200. 


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Army  Medical  Center  in  El  Paso,  TX. 

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SAIIMT  STVXrJISLALJS 

E 


OTOLARYNGOLOGY/ 

HEAD  & NECK  SURGERY  REPORT 


MENIERE’S  DISEASE: 

REVIEW  AND  UPDATE 

LORNA  BRASS,  MD;  PAUL  A.  BLAIR,  MD 


This  is  a brief  review  of  the  clinical  findings, 
pathology,  and  present  concepts  in  the  etiology  of 
Meniere's  disease.  There  is  a discussion  of 
evaluation  and  multiple  modes  of  therapy. 


Meniere's  Disease  is  a disease  affecting  the  inner 
ear.  The  hallmark  of  the  disease  is  the  triad  of 
symptoms:  vertigo,  tinnitus,  and  fluctuating  hearing 
loss.^  In  addition,  a sensation  of  fullness  in  the  ear  is 
common.  The  disease  has  been  reported  in  children 
(Hausler,  et  al)  but  usually  occurs  after  20  years  of 
age  and  rarely  after  60.^  Although  the  incidence  is  not 
precisely  known,  there  are  approximately  100,000  new 
cases  per  year  and  about  2.4  million  people  affected 
in  the  United  States.  The  disease  is  usually  unilateral 
but  up  to  20-30%  of  patients  will  eventually  have  in- 
volvement of  the  other  ear.  This  appears  to  be  more 
likely  in  individuals  whose  onset  of  Meniere's  disease 
is  later  in  life.  Patients  usually  have  most  or  all  of  the 
classic  findings  but,  occasionally,  one  symptom  pre- 
dominates or  precedes  the  others. 

The  disease  was  first  described  by  a French  phy- 
sician, Prosper  Meniere,  in  1861.  It  was  not  until  1938 
that  a probable  histopathology  was  known.  Hallpike 
and  Cairns  in  England,  as  well  as  Yamakawa  in  Japan, 
noted  hydropic  distention  of  the  endolymphatic  sys- 
tem.^ Despite  much  research,  the  pathogenesis  of 
Meniere's  disease  remains  unknown. 


JOURNAL  VOL  140  JULY  11 


CLINICAL  FINDINGS 

Vertigo 

This  is  the  most  distressing  and  disabling  of  the  symp- 
toms and  the  most  likely  to  cause  the  patient  to  seek 
medical  attention.  The  pattern  of  these  episodes  can 
be  quite  variable.  They  may  last  from  20  minutes  to 
several  hours  with  normal  equilibrium  between  epi- 
sodes. They  may  occur  with  greater  and  greater  fre- 
quency as  the  disease  progresses  and  then  begin  to 
decrease,  or  they  may  occur  in  clusters  with  long  pe- 
riods free  of  vertiginous  episodes.  The  episodes  may 
be  preceded  by  a sensation  of  aural  fullness  or  a greater 
decrease  in  hearing  and  may  be  accompanied  by  nau- 
sea and  vomiting,  prostration,  diaphoresis,  and  pal- 
lor. Although  the  "spell"  may  have  preliminary 
symptoms,  this  aura  is  never  accompanied  by  sei- 
zures, loss  of  consciousness,  paralysis,  or  dysarthria. 
As  the  episode  abates  (which  may  take  hours),  the 
patient  may  fall  asleep  and  upon  awakening  feel  to- 
tally normal.  There  is  no  postictal  phase.  There  may 
be  some  motion  intolerance  that  lasts  several  days. 
Hearing  on  the  affected  side  may  remain  decreased 
after  the  episode  but  is  occasionally  found  to  improve, 
a paradoxical  improvement  called  Lermoyez's  syn- 
drome. 

Two  other  patterns  of  vertiginous  spells  also  oc- 
cur. The  first,  lasting  only  a few  seconds,  usually 
brought  on  by  sudden  movement,  consisting  of  a mo- 
mentary loss  of  balance,  gives  the  appearance  of  an 
inebriated  gait.  The  second  type  of  spell  dubbed 
"fainting  spells  of  Tumerkin"  or  "Utricular  crises"  are 
short,  severe  episodes  of  vertigo  that  occur  without 
aura  or  warning.  The  patient  is  thrown  violently  to 
the  ground.  Again,  there  is  no  loss  of  consciousness 
and  these  drop  attacks  are  usually  brief. 

The  vertigo  of  Meniere's  disease  is  of  the  periph- 
eral type.  As  with  all  true  vertigo  there  is  a sense  of 
movement  either  of  the  patient,  or  of  his  surround- 
ings. This  peripheral  vertigo  is  characterized  by  sud- 
den onset,  short  duration,  paroxysmal  nature,  intense 
severity,  exacerbation  by  position  or  movement  often 
with  a latency,  and  fatiguability  if  the  sensation  is 
always  in  the  same  direction.  It  may  be  accompanied 
by  horizontal  nystagmus,  shifting  from  toward  the 
side  of  the  lesion  early  in  the  disease  process,  to  away 
from  the  lesion  side  later  in  the  course.  Other  otologic 
symptoms,  such  as  tinnitus  and  hearing  loss  as  well 

12  JOURNAL  VOL  140  JULY 


as  systemic  symptoms  of  nausea  and  vomiting  may 
occur  with  peripheral  vertigo.  Peripheral  vertigo  is  an 
indication  of  a lesion  in  the  semicircular  canals  or 
vestibular  nerve.  In  contradistinction,  central  vertigo 
is  an  indication  of  a lesion  of  the  vestibular  nuclei, 
the  vestibular  tracts  in  the  brain  stem,  the  cerebellum, 
or  the  cerebrum.  Central  vertigo  is  characterized  by 
slow  onset  lasting  days  to  months,  by  a more  contin- 
uous state,  and  by  less  severity.  Nystagmus  may  be 
horizontal,  rotary,  or  vertical  without  accompanying 
otologic  or  systemic  symptoms  but  possibly  accom- 
panied by  other  neurologic  symptoms. 

Tinnitus 

Tinnitus  of  Meniere's  disease  may  be  episodic  or  con- 
tinuous. It  does  not  have  a pulsatile  nature  nor  does 
it  change  with  change  in  carotid  pressure.  The  pitch 
tends  to  parallel  the  area  of  hearing  loss;  the  pitch  of 
the  tinnitus  is  low  if  the  hearing  loss  is  in  the  low 
frequencies. 

Hearing  Loss 

Auditory  acuity  changes  in  Meniere's  disease  are  of 
the  sensorineural  type  typical  of  cochlear  damage.  An 
acute  decrease  in  auditory  acuity  almost  always  ac- 
companies attacks  of  vertigo.  The  loss  is  fluctuating 
and  may  not  be  detected  at  the  early  stages  of  the 
disease.  If  the  disease  continues,  these  fluctuations 
in  hearing  become  less  obvious  and  are  replaced  by 
a steady  decrease  in  acuity.  Hyperacusis  is  usually 
present  secondary  to  recruitment.  In  addition,  the 
same  pitch  may  be  perceived  as  two  different  pitches 
by  the  two  ears,  known  as  diplacusis  binauralis  dys- 
harmonica  and  is  usually  higher  in  perceived  pitch  in 
the  affected  ear. 

Aural  Fullness 

This  disturbing  symptom  occurs  in  most  patients  with 
Meniere's  disease.  It  may  intensify  preceding  a ver- 
tiginous episode  but  is  usually  constant.  This  symp- 
tom may  be  the  first  symptom  noticed  in  the  pro- 
gression of  the  disease. 

ETIOLOGY 

Although  the  relationship  between  endolymphatic 
hydrops  and  Meniere's  disease  is  well  established, 
the  cause  of  this  disturbance  in  labyrinthine  fluids  is 
not  known.  Increase  in  endolymphatic  pressure  could 
be  secondary  to  over-production  or  under-resorption 


of  the  fluid.  Research  has  been  done  to  evaluate  pos- 
sible mechanical  obstruction  of  the  endolymphatic  duct 
or  the  vestibular  aqueduct,  or  possible  endolymphatic 
sac  abnormality.  Electrolyte  disorders  have  been  im- 
plicated with  specific  attention  to  potassium  and  cal- 
cium abnormalities.^'^  Endocrine  abnormalities  in- 
cluding hyperthyroidism,  pancreatic  insufficiency  and 
decreased  adrenal  function  have  been  reported  in 
Meniere's  patients  to  a greater  degree  than  in  the 
general  population.  Vascular  disease  in  the  form  of 
arterial  insufficiency,  anatomic  abnormalities,  or  ve- 
nous congestion  have  been  proposed  as  factors  in 
endolymphatic  hydrops.^'  ^ Autoimmune  disease  has 
been  implicated  with  type  II  reaction,  coUagen  anti- 
gen-antibody complexes  being  the  cause  of  initial 
damage.®  Evidence  of  increased  circulatory  complexes 
have  been  reported  by  some  researchers  but  refuted 
by  others.  XeneUis  found  a correlation  with  one  hu- 
man lymphocyte  antigen  group  but  other  evidence  of 
autoimmune  disease  was  lacking.^ 


AUergy  has  been  implicated  in  a small  percentage 
of  Meniere's  patients  (Stable).  The  proposed  mech- 
anism was  not  type  I antigen-antibody  mediated  but 
rather  an  alternate  definition  described  by  Rinkle, 
Bryant,  and  others. 

Finally,  certain  dependent  personality  types  are 
said  to  be  more  prone  toward  Meniere's  disease. 

With  etiology  stiH  unclear  but  pathophysiology 
accepted  most  therapies  are  based  on  correction  of 
the  pressure  shift  in  the  labyrinth  and  palliation  of 
symptoms. 

PATHOLOGY 

Endolymphatic  hydrops,  the  main  pathologic  finding 
in  Meniere's  disease,  can  be  described  as  swelling  of 
the  endolymph  containing  structures.  This  may  lead 
to  shift  in  the  central  structures  of  the  cochlea. 

Areas  of  localized  herniations  or  outpouching  can 
rupture  with  complete  healing  or  with  the  formation  ► 


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of  fistulas  between  the  endolymph  and  perilymph 
filled  spaces.  These  distortions  ultimately  lead  to  dys- 
function of  the  cochlea.  There  is  a loss  of  cochlear 
elements  only  occasionally;  hair  cells  and  ganglion 
cells  are  usually  normal  in  histology  and  number. 

PHYSICAL  EXAMINATION  AND 
FUNCTIONAL  TESTING 

Very  often,  there  are  no  unusual  findings  and  the 
general  physical,  neurological,  and  otologic  exami- 
nations are  within  normal  limits. 

Vestibular  Tests 

If  the  patient  is  tested  during  an  acute  vertiginous 
episode  nystagmus  is  always  present.  Electronystag- 
mogram  will  usually  demonstrate  nystagmus  with  the 
eyes  closed  for  several  days  after  an  episode.  The  most 
common  finding  is  hypoactivity  of  the  involved  lab- 
yrinth to  caloric  testing.  This  testing  may  also  precip- 
itate symptoms.  NadoP^  found  an  abnormal  fistula 
test  in  30%  of  patients  with  Meniere's  disease  and  this 
group  of  patients  appeared  more  reactive  to  negative 
pressure  than  to  positive  pressure. 

Audiography 

Pure  tone  audiograms  classically  show  a low  fre- 
quency sensorineural  hearing  loss,  but  progression  of 
the  hearing  loss  may  show  a flat  loss  throughout  the 
frequency  range.  Occasionally  upward  sloping  hear- 
ing loss  is  seen. 

Discrimination  scores  are  variable  but  are  usually 
in  the  range  appropriate  to  the  pure  tone  losses  dem- 
onstrated. 

Glycerol  Test 

Glycerol  administered  to  the  patient  acts  as  a diuretic. 
The  pure  tone  audiogram  is  checked  before  and  3 
hours  after  administration.  Serum  osmolality  is  also 
checked  to  make  sure  a diuretic  effect  is  achieved. 
Since  diuresis  theoretically  causes  a shift  in  the  coch- 
lear fluid  and  thus  a temporary  relief  of  the  endo- 
lympthatic  hydrops,  an  improvement  in  the  audi- 
ogram is  considered  diagnostic  of  Meniere's  disease; 
although  negative  results  do  not  rule  out  the  diag- 
nosis. This  test  must  be  administered  fairly  early  in 
the  course  of  the  disease. 

Electrocochleography 

While  not  used  at  most  centers,  electrocochleography 
14  JOURNAL  VOL  140  JULY 


TABLE  1 

CLASSIFICATION  OF  EFFICACY  OF  VARIOUS  THERAPIES 
FOR  MENIERE’S  DISEASE 

Class 

Results 

A 

Absence  of  definitive  vertiginous  spells  for 
the  described  period 
Hearing  improved. 

B 

Absence  of  definitive  vertiginous  spells  for 
the  described  period 
Hearing  unchanged. 

C 

Absence  of  definitive  vertiginous  spells  for 
the  described  period 
Hearing  worse. 

D 

Failure  to  control  definitive  spells. 

has  been  proposed  as  a means  to  select  patients  who 
may  go  on  to  develop  bilateral  disease.  Coats  and 
Kidder^^  found  68%  of  patients  with  Meniere's  disease 
had  an  abnormal  electrochochleogram  and  Coin,  et 
aP^  had  similar  results,  reporting  62%  of  Meniere's 
patients  had  an  abnormal  study. 

Auditory  Brainstem  Response 

Since  the  presenting  symptoms  and  audiogram  may 
not  be  discriminating  enough  to  separate  Meniere's 
disease  from  retrocochlear  disease  such  as  acoustic 
neuroma,  auditory  brainstem  response  is  the  screen- 
ing test  of  choice  to  separate  these  entities. 

THERAPY 

Treatment  of  Meniere's  disease  is  designed  to  either 
alter  the  course  of  the  disease  or  ameliorate  the  symp- 
toms. Various  committees  of  the  American  Academy 
of  Ophthalmology  and  Otolaryngology  have  estab- 
lished a scoring  system  to  compare  the  efficacy  of 
different  modalities  of  therapy  (Table  1). 

Medical  Therapy 

In  the  course  of  an  acute  vertiginous  attack,  control 
of  symptoms  is  usually  affected  using  sedatives,  an- 
tiemetics, and  vestibular  suppressants,  along  with  bed 
rest  and  appropriate  fluids. 

One  of  the  earliest  therapies  attempted  in  the 
treatment  of  the  vertigo  of  Meniere's  disease  was  ha- 
bituation.^^ Although  there  is  a physiologic  basis  for 
this  treatment,  the  episodic  nature  of  Meniere's  ver- 
tigo is  poorly  responsive  to  the  fatigue  effects  applied 


to  the  vestibular  system.  Thiazide  diuretics  with  po- 
tassium supplement  have  long  been  regarded  as  the 
best  initial  therapy.  Some  author's  have  advocated 
including  a low  salt  diet. 

Streptomycin  as  discussed  by  Moretz/®  has  been 
used  as  a vestibular  ablative  agent  in  patients  with 
I bilateral  disease,  where  preservation  of  hearing  is 
1 needed. 

j Local  infusion  of  aminoglycosides  into  the  laby- 
j rinth  has  also  been  advocated  by  Beck.^^ 

Other  medical  therapies  are  directed  at  specific 
! causes.  Allergy  therapy  and  immune  therapy  have 
been  tested  but  thus  far  have  not  proved  particularly 
I effective.  None  of  the  medical  therapies  has  appeared 
to  alter  the  natural  course  of  the  disease. 

; Surgical  Therapy 

Surgical  intervention  has  the  potential  to  prevent  or 
I reduce  progressive  labyrinthine  destruction.  Patient 
I selection  is  difficult  since  some  patients  will  have  a 


spontaneous  remission  or  respond  to  medical  ther- 
apy. 

Choice  of  operation  is  also  difficult.  Kitahara^° 
reports  on  18  years  of  experience  with  an  endolym- 
phatic sac  mastoid  shunt.  A total  of  78%  of  patients 
who  underwent  the  procedure  received  class  A re- 
sults. Hearing  was  worsened  in  only  15%  of  patients. 
For  those  undergoing  endolymphatic  sac-subarach- 
noid shunt  45-50%  showed  class  A or  B results  and 
30-40%  showed  class  D results  at  the  end  of  5 years. 
Smyth^  reports  73%  A or  B results  after  vestibular 
nerve  section  compared  to  5%  class  D results  with  6- 
to  56-month  foUow-up.  Comparing  vestibular  nerve 
section  to  saccus  decompression.  Primrose^  found  the 
former  to  be  far  superior  for  permanent  relief  of  ver- 
tigo. Similarly,  Boyce^^  reports  relief  of  vertigo  in  96% 
of  patients  who  underwent  retrolabyrinthine  vesti- 
bular nerve  resection.  Labyrinthectomy  is  still  done 
in  cases  of  intractable  vertigo  if  there  is  no  auditory 
activity  left  in  the  ear.  There  are  other  assorted  pro- 


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(504)  387-7900  In  Baton  Rouge 

CDU  of 

Willis-Knighton  South 

(318)  632-5111  In  Shreveport 

CDU  of  Lake  Charles 
Memorial  Hospital 

(Opening  Oct.  1, 1988) 


Affiliates  of  the  General  Health  System 
JCAHO  Accredited 


JOURNAL  VOL  140  JULY  15 


cedures  including  cryosurgery,  ultrasound,  trans- 
stapedial  tack  placement,  and  osmotic  induction  of 
the  round  window,  but  these  methods  have  generally 
fallen  out  of  favor. 

Complication  rates  for  most  of  these  procedures 
are  fairly  low  in  experienced  hands  and  are  similar  to 
those  in  patients  undergoing  mastoidectomy. 


SUMMARY 

Meniere's  disease  is  a process  of  variable  clinical  be- 
havior, with  spontaneous  remissions  or  steady  down- 
hill course,  of  single  episode  or  longstanding  dura- 
tion. 

The  etiology  of  this  disease  remains  elusive.  The 
body  of  knowledge  continues  to  grow  concerning 
possible  causes  and  contributing  factors. 

Effective  therapy  can  be  rendered  for  many  pa- 
tients if  a continuum  from  conservative  medical  ther- 
apy to  radical  surgery  is  considered  with  the  goal  of 
relief  of  distressing  symptoms  and  conservation  of 
function.  ■ 


HOWTO  FILE  A CLAIM  . . . 


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File  a claim  without 
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a paper  claim  form?  “ 

Certainly,  ELECTRONICALLY. 


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filing  physicians'  claims  simple  and  inexpen- 
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begin,  call  us  at  (504)  295-2085. 


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Keeping  One  Step  Ahead  . . . 


REFERENCES 

1.  Paparella  MM,  Shumrick  DA:  Otolaryngology.  New  York,  AB  Saunders, 
1980,  pp  1878-1888. 

2.  Hausler  R,  Toupet  M,  Guidetti  G,  et  al.  Meniere's  disease  in  children. 
Am  J Otolaryngol  1987;8(4):187-193. 

3.  Hallpike  C,  Cairns  SH:  Observation  on  the  pathology  of  Meniere's  dis- 
ease. / Laryngol  1938;53:625. 

4.  Meyer  zum  Gottesberge  AM,  Ninoyu  O:  A new  concept  in  pathogenesis 
of  experimental  hydrops:  Role  of  calcium.  Aviat  Spac  Environ  Med 
1987;58(9):A240-246. 

5.  Kanazuki  KE:  Vascular  loops  in  auditory  canal  as  possible  cause  of  Me- 
niere's disease  auris  nasus  Laryngoscope  1986;3(2):5105-5111. 

6.  Fukzawa  T,  Ohmura  MY:  The  effect  of  injection  of  high  K-l-  solution 
into  scala  media.  Acta  Otolaryngol  (Stockh)  1987;103(3-4):170-175. 

7.  Gussan  R:  Vascular  mechanisms  in  Meniere's  disease:  Theoretical  con- 
siderations. Arch  Otolaryngol  1982;108:544-546. 

8.  Yoo  TJ:  Etiopathogenesis  of  Meniere's  disease:  A hypothesis.  Ann  Otol 
Rhinol  Laryngol  1984;113  (Suppl):6-12. 

9.  Xenellis  J,  Morrison  AW,  McClowskey  D,  et  al.  HLA  antigens  in  the 
pathogenesis  of  Meniere's  disease.  / Laryngol  Otol  1986;100(1):2104. 

10.  Stable  J,  et  al:  Meniere's  disease  and  allergy  with  special  references  to 
immunoglobulin  and  IgE  antibody  (regin)  in  serum.  Equil  Res  1974;4:22- 
27. 

11.  Wexler  M,  Crary  WG:  Meniere's  disease:  The  psychosomatic  hypothesis. 
Am  J Otol  1986;7(2):93-96. 

12.  Nadol  JB:  Positive  Hennebert's  sign  in  Meniere's  disease.  Arch  Otolar- 
yngol 1977;103:524-530. 

13.  Skalabrin  TA,  Margham  CA:  Analysis  of  the  glycerin  test  for  Merviere's 
disease.  Otolaryngol  Head  Neck  Surg  1987;96(3):282-288. 

14.  Coats  A,  Kidder  H:  The  summating  potential  and  Meniere's  disease:  I 
Summating  potential  amplitude  in  Meniere's  and  non-Meniere's  ears. 
Arch  Otolaryngol  Head  Neck  Surg  1981;107:199-208. 

15.  Goin  D,  Stoller  S,  Asether  D,  et  al:  Summating  potential  in  Meniere's 
disease.  Laryngoscope  1982;92:1383-1389. 

16.  Norr  ME,  DeWeerdt  W:  Treatment  of  vertigo  based  on  habituation.  Phy- 
sio-pathological basis.  / Laryngol  Oto  1980;94(7):689-96. 

17.  Van  Deelen  GW,  Huizing  EH:  Use  of  diuretic  (Dyazide®)  in  the  treat- 
ment of  Meruere's  disease.  A double  blind  cross-over  placebo  controlled 
study.  ORL  ] Otorhinolaryngol  Relat  Spec  1986;48(5):281-292. 

18.  Moretz  WH  Jr,  Shea  JJ  Jr,  Orchik  DJ,  et  al:  Streptomycin  treatment  in 
Meniere's  disease.  Otolaryngol  Head  Neck  Surg  1987;96(3):256-259. 

19.  Beck  C:  Intratympanic  application  of  gentamydn  for  treatment  of  Me- 
niere's disease.  Keio  } Med  1986;35(1):36-41. 

20.  Kitahara  M,  Katajima  K,  Yazawa  Y,  et  al:  Endolymphatic  sac  surgery 
for  Meniere's  disease:  Eighteen  years  experience  with  the  Kitahara  sac 
operation.  Am  J Otol  1987;8(4):283-286. 

21.  Brackman  DE,  Nissen  RL:  Meniere's  disease.  Results  of  treatment  with 
endolymphatic  subarachnoid  shunt  compared  with  endoylmphatic  mas- 
toid shunt.  Am  J Otol  1987;8(4):275-282. 

22.  Smyth  GD,  Kerr  AG,  Gordon  DS,  et  al:  Vestibular  nerve  section  for 
Meniere's  disease.  J Laryngol  Otol  1976;80:823-831. 

23.  Primrose  WJ,  Smyth  GD,  Kerr  AG,  et  al:  Vestibular  nerve  section  and 
saccus  decompression:  An  evaluation  of  long  term  results.  / Laryngol  Otol 
1986;100(7)775-784. 

24.  Boyce  SE,  Mischke  RE,  Goin  DW:  Hearing  results  and  control  of  vertigo 
after  retrolabyrinthine  vestibular  nerve  section.  Laryngoscope  1988;8(3):257- 
261. 


Dr  Brass  is  a resident  in  the  Dept  of  Otolaryngology  — Head  and  Neck 
Surgery  at  Tulane  University  Medical  Center  in  New  Orleans. 

Dr  Blair  is  otolaryngologist  and  facial  plastic  surgeon  in  New  Orleans. 
He  is  also  a professor  in  the  Dept  of  Otolaryngology  — Head  and  Neck 
Surgery  at  Tulane  University  Medical  Center. 


16  JOURNAL  VOL  140  JULY 


1 


Jackie  Tucker,  LSMSA  President 


AUXILIARY  REPORT 


LUNGS  FOR  LIFE 

REBECCA  BOMBET  BASILE 


WHEN  YOU  consider  that  cigarette  smoking  is  re- 
sponsible for  approximately  83%  of  all  lung  can- 
cer and  30%  of  all  cancer-related  deaths,  you  might 
ask  yourself  why?  Why  do  people  smoke? 

Take  a minute  and  reflect  on  several  current  US 
statistics.  One  in  every  five  high  school  seniors  smokes 
daily.  Of  teenagers,  10%  smoke.  Most  teenagers  begin 
smoking  before  age  16.  Most  teenagers  decide  to  smoke 
by  the  sixth  or  seventh  grade. 

Other  facts  to  consider  include; 

• There  have  been  recent  trends  in  smokeless  tobacco 
which  correlate  with  increase  in  neoplasmas  and 
other  disorders  of  the  mouth  and  throat  frequently 
seen  in  young  male  adolescents. 

• An  estimated  136,000  deaths  were  related  to  limg 
cancer  in  1987.  The  age-standardized  lung  cancer 
death  rate  for  women  is  higher  than  that  of  any  other 
cancer.  It  has  surpassed  cancer  of  the  breast  which 
was  the  number  one  cancer  kiUer  in  women  for  more 
than  50  years. 

• Those  who  smoke  two  or  more  packs  of  cigarettes 
per  day  have  a lung  cancer  mortality  rate  15  to  20 
times  greater  than  non-smokers. 


• Smoking  is  related  to  320,000  deaths  per  year  with 
an  estimated  cost  from  38  to  95  billion  dollars. 

It  is  said  that  cigarette  smoking  is  the  largest  sin- 
gle preventable  cause  of  premature  death  and  disa- 
bility in  the  United  States.  With  all  of  this  information 
so  readily  available,  again,  why  do  people  smoke? 

In  the  fall  of  1986  the  St  Landry  Parish  Medical 
Auxiliary  began  to  evaluate  this  information.  The 
American  Medical  Association  (AMA)  and  AMA  Aux- 
iliaries had  recently  begun  an  Antismoking  Public  Serv- 
ice Campaign  promoting  their  policy  of  a smoke-free 
society  by  the  year  2000.  The  auxiliary  decided  to 
promote  this  campaign  on  a local  level  by  creating 
and  providing  a smoking  education  program  for  the 
parish  youth.  After  joining  forces  with  two  of  the  local 
hospM  pulmonary  rehabilitation  programs,  the  re- 
search began.  Many  available  resources  were  evalu- 
ated and  the  age  group  to  be  targeted  was  deter- 
mined. 

Since  the  decision  to  smoke  is  usually  made  by 
the  sixth  or  seventh  grade,  the  educational  program 
was  presented  to  fourth,  fifth,  and  sixth  graders  only. 
After  reviewing  several  films,  the  film  "'Why  People  ► 

JOURNAL  VOL  140  JULY  19 


Smoke"  was  chosen,  and  was  purchased  with  funds 
provided  by  the  St  Landry  Parish  Medical  Society. 
This  is  a 10-minute  color  cartoon  depicting  four  rea- 
sons why  people  smoke.  Once  the  film  was  acquired 
and  a one-hour  presentation  was  developed,  the  pro- 
gram was  presented  to  the  St  Landry  School  Board 
representative  who  authorized  use  of  the  program  in 
the  parish  schools. 

The  presentation  consisted  of  an  introduction 
which  included  information  on  the  sponsors,  a brief 
review  of  lung  and  heart  anatomy,  facts  and  statistics 
on  smoking,  a teenage  smoker's  profile,  a short  dem- 
onstration with  plastic  lungs  and  a cigarette,  the  film, 
and  a period  for  questions  and  answers.  It  was  con- 
cluded with  a song  by  the  American  Heart  Association 
titled,  "Smoke  Is  No  Joke."  The  children  were  given 
several  handouts,  including  the  words  to  the  song. 

The  auxiliary  had  decided  to  form  teams  of  two, 
with  one  person  to  give  the  presentation  and  the  other 


AMA/NET  Simplifies  the  Task 
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sponsored  by  the  AMA,  it's  easy  to  keep  up  with  the  latest 
clinical  and  biomedical  literature,  health  care  business 
information  and  medical  news.  You  can  access  the 
information  you  need.  . . when  you  need  it.  . . with  just 
your  computer,  a modem  and  your  phone.  No  computer 
expertise  .required! 

■ Literature  Searches 

EMPIRES/Excerpta  Medica  • Disease  Information 
MEDLINE  • Social  & Economic  Aspects  of  Medicine 

■ Associated  Press  Medical  News  Service 

■ Professional  Programs 

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physician's  diagnostic  considerations.  From  the 
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Sponsored  by  the  American  Medical  Association. 

AMA/NET  IS  a service  of  SoftSearch,  Inc.  and  American  Medical  Computing.  Ltd.,  a subsidiary  of  the  AMA 


person  to  distribute  the  information  and  handle  the 
audio  and  video  equipment.  Eight  teams  were  formed 
which  included  nurses  from  the  rehabilitation  pro- 
grams at  both  hospitals.  It  was  the  auxiliary's  goal  to 
visit  one  half  of  the  parish  schools  the  first  year  and 
the  other  half  the  following  year.  Once  all  the  schools 
had  been  visited,  the  auxiliary  would  only  visit  all 
fourth  graders  on  a yearly  basis.  Each  team  visited 
two  or  three  schools  and  were  responsible  for  coor- 
dinating the  program  with  their  schools. 

The  auxiliary  named  the  program  Lungs  for  Life 
. . . explaining  to  the  children  that  everyone  gets  only 
one  set  of  lungs,  which  makes  it  very  important  to 
have  all  the  facts  before  one  decides  to  start  smoking. 
A logo  was  designed  using  a simple  outline  of  the 
lungs  and  was  used  on  all  literature  given  out  as  well 
as  t-shirts  that  were  made  for  the  auxiliary  to  wear 
when  they  went  to  the  schools.  The  t-shirts  were  so 
popular  with  the  children  that  the  auxiliary  obtained 
permission  from  the  school  board  to  sell  the  shirts  in 
the  schools  with  the  profit  going  back  into  the  pro- 
gram. 

The  auxiliary  plans  to  add  a new  aspect  to  the 
program  this  year.  Several  high  school  juniors  and 
seniors  will  become  part  of  our  team.  They  will  not 
only  help  with  the  presentation  but  will  also  help  sell 
the  t-shirts  in  the  school.  It  is  felt  that  this  will  serve 
as  positive  role  models  for  the  younger  children  and 
positive  peer  pressure  in  the  high  schools. 

The  program,  in  its  second  year,  has  been  quite 
successful.  It  has  been  positively  received  both  by  the 
schools  and  the  children  and  the  community.  The 
auxiliary  has  been  invited  to  participate  in  parades 
and  health  fairs.  The  Girl  Scouts  have  asked  for  the 
program  as  well  as  other  groups. 

Today  there  are  over  40  million  nonsmokers  in 
the  United  States.  Education  is  the  key  factor  in  this 
healthy  change.  If  we  want  to  impact  the  future  adults 
of  this  country,  then  the  best  place  to  start  is  with 
our  children  . . . which  is  what  our  auxiliary  is  doing. 

And  we  are  telling  them  . . . "Smoke  is  no  joke." 


Mrs  Basile  (wife  of  Michael  W.  Basile,  MD)  is  the  president  of  the  St 
Landry  Parish  Medical  Society  Auxiliary  and  the  Community  Relations 
Health  Coordinator  at  Opelousas  General  Hospital. 


20  JOURNAL  VOL  140  JULY 


♦♦♦the  Cornerstone 
of  Our  Professions 


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concern  manifested  in  the 
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make  to  aid  him  in  recovery. 
After  all,  caring  is  the 
cornerstone  of  your  practice. 

Occasionally  a company 
appears  with  the  same  caring 
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serve  the  doctor.  In  the  field  of 
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that  company  is  Insurance 
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you,  we  make  caring  for  our 
insured  the  cornerstone  of  our 
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THE  FIVE  HORSEMEN  OF 
RHEUMATOLOGY 


JACK  WAXMAN,  MD 


24  JOURNAL  VOL  140  JULY 


The  aging  musculoskeletal  system  is  prone  to 
painful  articular  and  para-articular  syndromes 
which  mimic  one  another  with  similar  historical 
and  physical  clues.  The  physician's  tendency  is  to 
lump  these  overuse  conditions  together  and 
provide  a nonsteroidal  anti-inflammatory  drug  for 
therapy.  Herein  are  the  clues  to  effectively 
differentiate  these  five  "itises"  and  thus  manage 

them  more  specifically. 

Five  rheumatologic  ills  tend  to  occur  in  the  aged 
patient  group,  and  often  several  appear  in  the  same 
individual.  The  five  "itises"  are  osteoarthritis,  bur- 
sitis, tendinitis,  neuritis,  and  fibrositis.  Separating 
them  can  be  quite  challenging;  nevertheless,  it  is  im- 
portant since  management  of  each  differs.  For  the 
most  part,  they  are  painful  joint  and  para-articular 
syndromes  based  on  overuse,  abuse,  or  obesity  with 
too  many  repetitions  or  too  much  load  exerted  upon 
tendons,  bursae,  or  joints.  In  fibrositis,  however,  ex- 
cess pain  in  muscles  occurs  via  sleep  deprivation,  anx- 
iety, and  depression.  An  underlying  "itis"  is  also 
present  in  the  majority  of  fibrositis  patients  who  are 
thus  considered  to  have  "secondary"  fibrositis  as  op- 
posed to  the  less  common  primary  disease.^  Osteoar- 
thritis and  especially  fibrositis  (90%)  are  more  com- 
mon in  females,  with  menopausal  aggravation 
common  to  both  ills. 

OSTEOARTHRITIS 

In  osteoarthritis,  20  years  of  joint  impulse  loading 
leads  to  fibrillation,  cartilage  loss,  spur  formation,  and 
increased  capsular  thickening  of  multiple  joints,  es- 
pecially distal  finger  joints,  knees,  hips,  neck,  and 
back.  There  is  a secondary,  usually  modest  but  oc- 
casionally intense,  inflammatory  response  based  on 
cartilaginous  debris  and/or  crystalline  deposition.  Pain 
after  joint  use  is  common,  especially  by  evening,  but 
morning  stiffness  is  usually  for  less  than  15  minutes. 
Tenderness  is  prominent  at  the  worn-down  area  of 
the  joint  (for  example,  a medial  joint  line  of  the  knee 
or  the  lateral  patellofemoral  grove)  with  local  crepi- 
tation on  movement.  An  x-ray  film  will  often  reveal 
definite  arthritis  even  though  only  50%  (or  less)  of 
radiographically  visible  osteoarthritic  sites  are  symp- 
tomatic. 

In  management,  first  take  care  to  exclude  the  other 


"itises,"  which  can  rnirnic  osteoarthritis  by  similar  post 
work  pain,  and  then  prescribe  joint  rest,  isometric 
muscle  strengthening,  weight  loss,  and  an  episodic 
anti-inflammatory  regimen  keyed  to  the  overuse  pat- 
terns. 

TENDINITIS  AND  BURSITIS 

Mimicry  of  osteoarthritis  commonly  occurs  at  the 
shoulder  and  hip  where  the  more  common  painful 
syndromes  are  rotator  cuff  tendinitis  with  associated 
subdeltoid  bursitis  and  gluteal  tendinitis  with  tro- 
chanteric bursitis.  Tenderness  upon  palpation  local- 
izes soreness  at  the  lateral  subacromial  margin  in  the 
former  condition  and  at  the  trochanter  in  the  latter. 

In  trochanteric  bursitis,  pain  spreads  laterally  down 
the  limb  and  usually  stops  at  the  next  joint;  occasion- 
ally, however,  it  goes  beyond  this  point  to  the  ankle. 
There  is  restriction  of  external  rotation  in  both  con- 
ditions, but  internal  rotation  is  more  limited,  partic- 
ularly in  hip  osteoarthritis. 

At  the  elbow,  tendinitis  usually  occurs  laterally 
at  the  epicondyle,  while  bursitis  occurs  posteriorly  at 
the  olecranon  and  may  be  septic  (Staphylococcus  au- 
reus), gouty,  or  traumatic.  At  the  knee,  bursitis  occurs 
anteriorly  or  posteriorly  (anserine  and  prepatellar  or 
gastrocnemius),  the  latter  mimicking  phlebitis  be- 
cause knee  fluid  extends  posteriorly  into  the  bursal 
sac  which  communicates  with  the  joint  in  two  thirds 
of  patients.  Eventually  such  extension  may  rupture 
into  the  calf  with  the  full-blown  phlebitic  syndrome 
reproduced.  Knee  tendinitis,  especially  in  runners,  is 
lateral  and  occurs  at  the  insertion  of  the  popliteus 
above  the  joint  line,  at  the  iliotibial  tract  at  its  tibial 
insertion,  or  at  the  patellar  tendon  insertion  in  sports 
that  include  jumping.^  At  the  ankle,  the  Achilles  ten- 
don is  vulnerable,  while  in  the  foot  or  leg  the  posterior 
tibial  tendon  origin  or  insertion  may  tear  with  pain 
on  overuse,  particularly  in  runners.  Knowing  the  ex- 
act site  of  these  tendon  origins  and  insertions  allows 
definition  by  carefully  palpating  for  the  often  tiny 
tender  site.  Resisted  isometric  contraction  also  allows 
reproduction  of  the  pain  and  separates  it  from  os- 
teoarthritis. 

Treatment  for  these  painful  syndromes  again  em- 
phasizes reduced  use,  ice  for  superficial  inflammatory 
sites,  anti-inflammatory  regimens  when  ice  is  not  suf- 
ficient, and/or  local  steroid  administration  adjacent  to  ► 


JOURNAL  VOL  140  JULY  25 


the  inflammatory  focus.  A re-strengthening  of  the  in- 
volved muscle  groups  and  a re-stretching  of  the  ten- 
don as  it  heals  is  important  because  loss  of  motion 
from  the  bound-down  tendon-bursal  complex  is  com- 
mon and  impedes  rehabilitation.  This  is  particularly 
important  at  the  shoulder,  which  loses  most  motion 
and  where  a ''frozen  shoulder"  is  likely  if  there  is 
significant  delay  in  re-stretching  maneuvers. 

NEURITIS 

Neuritis  also  mimics  the  preceding  syndromes,  par- 
ticularly at  the  shoulder  and  hip  where  C-6  and  C-7 
root  lesions  and  L-4,  L-5,  and  S-1  root  syndromes 
cause  nerve  or  muscle  pain  in  similar  distributions. 
Attention  to  distal  paresthesias  or  frankly  numb  fin- 
gers and  toe  tips  helps  prove  the  nerve  origin  of  the 
more  proximal  pain  state.  In  particular,  an  L4-5  disc 
abutting  the  L5  root  simulates  trochanteric  bursitis  by 
causing  lateral  thigh  and  leg  pain.  Careful  examina- 
tion of  the  sore  L-4  and  L-5  spinous  processes  and 
gluteal  musculature  locates  the  origin  of  this  neuro- 
pathy. Another  important  clue  is  that  first  toe  dor- 
siflexion  strength  and  straight  leg  raising  tests  are 
usually  abnormal,  particularly  in  a seated  position. 

Therapy  of  nerve  root  syndromes  is  based  on 
protecting  the  nerves  from  further  entrapment  or 
pressure  by  the  use  of  proper  posture  or  traction. 
Often,  collar  or  corset  supports,  or  even  maximal  pro- 
tection with  bedrest  is  required.  Weeks  or  even  months 
of  slow  healing  is  the  rule,  as  is  also  true  for  tendinitis, 
and  the  patient  must  avoid  returning  to  routine  ac- 
tivities too  soon  as  this  reaggravates  the  condition. 

FIBROSITIS 

Fibrositis  patients  are  separated  from  the  above  pained 
individuals  by  a more  persistent,  virtually  continuous 
pain  state  that  tends  to  be  diffuse,  symmetric,  and 
tends  to  be  inclusive  of  an  average  of  12  "tender" 
points.  These  excessively  sore  muscle  bellies  or  ten- 
don insertions  cause  marked  patient  withdrawal  or 
recoil  on  gentle  palpations.  These  patients  have  trou- 
ble getting  and  staying  asleep,  and  are  often  psycho- 
logically disturbed  with  chronic  depression  and  anx- 
iety, making  management  difficult.  Two  out  of  three 
are  menopausal  before  they  are  fibrositic,  and  their 
menopause  is  usually  premature  and  often  surgical.^ 

Therapy  focuses  early  on  physical  muscle  ther- 
apies, especially  heat  (occasionally  ice  before  stretch) 

26  JOURNAL  VOL  140  JULY 


with  massage  and  mobilizing  techniques,  and  then 
later  on  conditioning  exercises.  Tricyclics  are  com- 
monly prescribed  for  sleep;  psychotherapy  and  estro- 
gen may  be  necessary  as  well.  If  the  other  underlying 
"itises"  contribute  to  the  painful  state,  they  must  also 
be  managed.  Despite  all  these  efforts,  chronic  pain  is 
still  the  rule,  with  only  partial  therapeutic  success 
during  months  or  years  of  treatment. 

The  older  patient  who  presents  with  one  or  more 
joint  complaints  without  swelling,  with  normal  sedi- 
mentation rate,  and  with  the  changes  of  osteoarthritis 
on  joint  x-ray  films  presents  a challenge  to  the  ex- 
amining physician.  He  must  consider  four  other  re- 
lated syndromes  and  differentiate  them  by  exami- 
nation techniques  and  historical  clues.  This  may  be  a 
tedious  process  and  is  often  bypassed  in  the  rushed 
world  of  medicine,  but  treatments  of  these  states  will 
vary  and  follow-up  will  be  crucial  in  healing  these 
disorders.  Moreover,  since  these  "five  horsemen"  ride 
together,  modification  of  initial  therapy  plans  to  in- 
clude treatments  for  other  "itises"  may  well  be  nec- 
essary. The  examining  physician  should,  therefore, 
resist  the  impulse  to  simply  provide  an  anti-inflam- 
matory drug  for  these  painful  states.  Although  such 
a drug  may  be  helpful,  it  will  not  do  justice  to  the 
problems  these  syndromes  pose.  ■ 

REFERENCES 

1.  Wolfe  F,  Cathey  M:  Prevalence  of  primary  and  secondary  fibrositis.  / 
Rheumatol  1982;10:965-968. 

2.  Brody  DM:  Running  injuries.  Clin  Symp  1980;32:15. 

3.  Waxman  J,  Zatzkis  SM:  Fibromyalgia  and  menopause.  Postgrad  Med 
1986;80:165-171. 


Dr  Waxman  is  from  the  Dept  of  Internal  Medicine,  Section  on 
Rheumatology  at  Ochsner  Clinic  and  Alton  Ochsner  Medical 

Foundation  in  New  Orleans. 

Reprint  requests  should  be  sent  to  Dr  Waxman, 
1514  Jefferson  Highway,  New  Orleans,  LA  70121. 


KAWASAKI’S  SYNDROME 
ACCOMPANIED  BY  BONE  MARROW 

SUPPRESSION 


IRWIN  COHEN,  MD;  MICHAEL  WHISTLER,  MD 


This  article  reports  for  the  first  time  a 
simultaneous  occurrence  of  bone  marrow 
suppression  and  Kawasaki's  syndrome  (KS). 
Whereas  a granulocytosis  and  thrombocytosis 
usually  accompany  KS,  our  patient  experienced  a 
profound  neutropenia  and  thrombocytopenia. 
Although  the  case  fulfilled  the  Centers  for  Disease 
Control  clinical  criteria  for  KS,  these  labortory 
findings  so  confounded  the  diagnostic  skills  of  the 
attending  physicians  that  coronary  aneurysms  were 
not  looked  for  until  late  in  the  illness.  It  is  likely 
that  the  confusion  was  caused  by  the  effects  of 
drug  allergy  on  laboratory  derived  data.  The 
diagnosis  of  KS  is  still  a clinical  one. 


SINCE  ITS  FIRST  description  by  Kawasaki,  et  aP  in 
1967  and  again  in  1974,  acute  mucocutaneous 
lymph  node  syndrome,  or  Kawasaki's  syndrome  (KS) 
has  been  increasingly  recognized  in  this  country.^- ^ 
The  syndrome  is  that  of  an  acute,  febrile  illness  of 
young  children  with  characteristic  manifestations  as 
defined  by  the  Centers  for  Disease  Control  (CDC).^ 
Common  laboratory  findings  include  polymorpho- 
nuclear leucocytosis  and  thrombocytosis.^  We  re- 
cently encountered  a case  of  KS  with  bone  marrow 
suppression.  To  our  knowledge,  this  concurrence  has 
never  been  reported. 

CASE  REPORT 

A 9-month-old  black  infant  boy  who  was  well  until 
8/12/86  when  he  was  taken  to  his  pediatrician  with  a 
one-day  history  of  fever.  His  temperature  was  40.1°C. 
A diagnosis  of  acute  otitis  media  was  made;  he  was 
sent  home  on  a combination  of  amoxacillin  and  cla- 
vulanic  acid.  After  two  doses  he  developed  an  urti- 
carial rash.  The  following  day,  illness  day  (ID)  3,  still 
febrile,  he  was  taken  back  to  his  pediatrician.  The  CBC 
was  normal;  CSF  culture,  blood  culture,  and  serum 


JOURNAL  VOL  140  JULY  31 


specify  Adjunctive. 


latex  agglutination  tests  were  normal.  Medication  was 
changed  to  a combination  of  erythromycin  and  sul- 
fasoxazole.  Over  the  next  two  days  his  fluid  intake 
decreased  and  he  developed  diarrhea.  On  ID  5,  he 
was  admitted  to  a private  hospital  for  treatment  of 
dehydration  and  fever.  His  sclerae  were  injected.  His 
blood  picture  showed  a hemoglobin  of  10.7  g/dL,  a 
hematocrit  of  33.3%,  a white  cell  count  of  13,100  with 
a differential  of  65%  polymorphonuclears,  20%  bands, 

9%  lymphocytes,  3%  monocytes,  2%  eosinophils,  and 
1%  metamyelocytes  and  a platelet  count  of  294,000. 
Intravenous  fluids  and  cefuroxime  therapy  at  100  mg/ 
kg/day  were  started.  The  following  day  gentamicin, 

7 mg/kg/day,  was  added  because  of  persistent  fever, 
abdominal  distention,  and  scrotal  swelling.  A repeat 
lumbar  puncture  was  performed  with  CSF  findings 
of  protein  20  mg/dL,  glucose  72  mg/dL,  12  WBCs  and 
3 RBCs.  CSF  culture  and  Hemophilus  influenza  latex 
agglutination  test  were  negative;  the  platelet  count 
had  fallen  to  140,000.  On  ID  9,  the  cefuroxime  was 
increased  to  200  mg/kg/day.  On  ID  11,  he  was  still 
febrile;  had  developed  edema  of  his  hands  and  feet 
and  a generalized  maculopapular  eruption.  The 
hemoglobin  level  had  dropped  to  7.1  g/dL;  the  he- 
matocrit was  21.5%;  the  platelet  count  was  36,000;  and 
the  reticulocyte  count  was  0.1%;  the  white  cell  count 
of  20,200;  and  a differential  cell  count  showed  49% 
polymorphonuclears,  3%  bands,  43%  lymphocytes, 
and  5%  monocytes.  Gentamicin  and  cefuroxime  were 
stopped  and  the  patient  was  transferred  to  Tulane 
Medical  Center. 

At  Tulane,  on  ID  11,  his  temperature  was  39°C. 

His  lips  were  red  and  there  were  perioral  fissures.  He 
had  a diffuse  erythematous  rash  with  target  lesions 
on  his  hands  and  face.  His  feet  were  edematous  and 
his  scrotum  was  swollen.  There  was  a small  testicular 
hydrocele.  Some  small,  bilateral  axillary  nodes  were 
noted  but  no  cervical  adenopathy.  Laboratory  studies 
showed  a hemoglobin  level  of  6.7  g/dL;  a hematocrit 
of  21.1%;  a platelet  count  of  20,000;  a white  cell  count 
of  12,800;  a differential  cell  count  of  11%  polymor- 
phonuclears, 8%  bands,  75%  lymphocytes,  and  6% 
monocytes;  and  an  erythrocyte  sedimentation  rate  of 
55  mm/hr.  Both  antiplatelet  and  antigranulocyte  an- 
tibodies were  present.  C3  and  C4  were  depressed.  A 
urinalysis  showed  40-50  WBC/HPF  but  a negative  cul- 
ture. Other  negative  studies  included:  viral  cultures, 
antibody  and  antigen  for  hepatitis  A and  B viruses, 
antibody  for  Epstein-Barr  virus  and  cytomegalovirus,  ^ 

32  JOURNAL  VOL  140  JULY 


Each  capsule  contains  5 mg  cblordiazepoxide  HCl  and  2.5  mg  clidinium 
bromide. 

Please  consult  complete  prescribing  information,  a summary  of  which  follows: 


* Indications:  Based  on  a review  of  this  drug  by  the  National  Academy  of 
Sciences— National  Research  Council  and/or  other  information,  FDA  has 
classified  the  indications  as  follows: 

"Possibly”  effective:  as  adjunctive  therapy  in  the  treatment  of  peptic  ulcer 
and  in  the  treatment  of  the  irritable  bowel  S5mdrome  (irritable  colon,  spastic 
colon,  mucous  colitis)  and  acute  enterocolitis. 

Final  classification  of  the  less-than-effective  indications  requires  further 
investigation. 


Contraindications:  Glaucoma;  prostatic  hypertrophy,  benign  bladder  neck 
obstruction;  hypersensitivity  to  cblordiazepoxide  HCl  and/or  clidinium  Br. 
Warnings:  Caution  patients  about  possible  combined  effects  with  alcohol  and 
other  CNS  depressants,  and  against  hazardous  occupations  requiring  complete 
mental  alertness  (e.g.,  operating  machinery,  driving). 

Usage  in  Pregnancy:  Use  of  minor  tranquilizers  during  first  trimester 
should  almost  always  be  avoided  because  of  increased  risk  of  congeni- 
tal malformations  as  suggested  in  several  studies.  Consider  possibility 
of  pregnancy  when  instituting  therapy.  Advise  patients  to  discuss 
therapy  if  they  intend  to  or  do  become  pregnant. 

As  with  aU  anticholinergics,  inhibition  of  lactation  may  occur. 

Withdrawal  symptoms  of  the  barbiturate  type  have  occurred  after  discontinuation 
of  benzodiazepines  (see  Drug  Abuse  and  Dependence). 

Precautions:  In  elderly  and  debilitated,  limit  dosage  to  smallest  effective  amount 
to  preclude  ataxia,  oversedation,  confusion  (no  more  than  2 capsules/day  initially; 
increase  gradually  as  needed  and  tolerated) . Though  generally  not  recommended, 
if  combination  therapy  with  other  psychotropics  seems  indicated,  carefully  con- 
sider pharmacology  of  agents,  particularly  potentiating  drugs  such  as  MAO  inhib- 
itors, phenothiazines.  Observe  usual  precautions  in  presence  of  impaired  renal  or 
hepatic  function.  Paradoxical  reactions  reported  in  psychiatric  patients.  Employ 
usual  precautions  in  treating  anxiety  states  with  evidence  of  impending  depres- 
sion; suicidal  tendencies  may  be  present  and  protective  measures  necessary. 
Variable  effects  on  blood  coagulation  reported  very  rarely  in  patients  receiving  the 
drug  and  oral  anticoagulants;  causal  relationship  not  established.  Inform  patients 
to  consult  physician  before  increasing  dose  or  abruptly  discontinuing  this  drug. 
Adverse  Reactions:  No  side  effects  or  manifestations  not  seen  with  either  com- 
pound alone  reported  with  Librax.  When  cblordiazepoxide  HCl  is  used  alone, 
drowsiness,  ataxia,  confusion  may  occur,  especially  in  elderly  and  debilitated; 
avoidable  in  most  cases  by  proper  dosage  adjustment,  but  also  occasionally 
observed  at  lower  dosage  ranges.  Syncope  reported  in  a few  instances.  Also 
encountered:  isolated  instances  of  skin  eruptions,  edema,  minor  menstrual  irreg- 
ularities, nausea  and  constipation,  extrapyramidal  symptoms,  increased  and 
decreased  libido— aU  infrequent,  generally  controUed  with  dosage  reduction; 
changes  in  EEG  patterns  may  appear  during  and  after  treatment;  blood  dyscrasias 
(including  agranulocytosis),  jaundice,  hepatic  dysfunction  reported  occasionally 
with  cblordiazepoxide  HCl,  making  periodic  blood  counts  and  liver  function  tests 
advisable  during  protracted  therapy.  Adverse  effects  reported  with  Librax  typical 
of  antichoUnergic  agents,  i.e.,  dryness  of  mouth,  blurring  of  vision,  urinary  hesi- 
tancy, constipation.  Constipation  has  occurred  most  often  when  Librax  therapy  is 
combined  with  other  spasmolytics  and/or  low  residue  diets. 

Drug  Abuse  and  Dependence:  Withdrawal  symptoms  similar  to  those  noted  with 
barbiturates  and  alcohol  have  occurred  foUowing  abrupt  discontinuance  of  chlor- 
diazepoxide;  more  severe  seen  after  excessive  doses  over  extended  periods;  milder 
after  taking  continuously  at  therapeutic  levels  for  several  months.  After  extended 
therapy,  avoid  abrupt  discontinuation  and  taper  dosage.  Carefully  supervise 
addiction-prone  individuals  because  of  predisposition  to  habituation  and 
dependence. 

p.l.  0288 

Roche  Products 


Roche  Products  Inc. 
Manati,  Puerto  Rico  (X)701 


When  it's  brain  versus  bowel, 


ITS  TIME 
HMITHE 


In  irritable  bowel  syndrome,*  intestinal 
discomfort  will  often  erupt  in  tandem  with 
anxiety— launching  a cycle  of  brain/bowel 
conflict.  Make  peace  with  Librax.  Because  of 
possible  CNS  effects,  caution  patients  about 
activities  requiring  complete  mental  alertness. 

*Librax  has  been  evaluated  as  possibly  effective 
as  adjunctive  therapy  in  the  treatment  of  peptic 
ulcer  and  IBS. 


Specify  Adjunctive 


Each  capsule  contains  5 mg  chlordiazepoxide 
HCl  and  2.5  mg  cUdinium  bromide. 


Copyright  ©1988  by  Roche  Products  Inc.  All  rights  reserved. 


Please  see  summary  of  prescribing  information  on  adjacent  page. 


antinuclear  antibody,  Coombs'  test,  stool  culture,  and 
stool  hematest.  A bone  marrow  aspiration  and  biopsy 
performed  on  ID  12  showed  an  increased  number  of 
megakaryocytes  with  suppression  of  both  the  eryth- 
rocyte and  granulocyte  precursors,  and  plasmacyto- 
sis. 

Fever  persisted  until  ID  23.  The  rash  resolved  on 
ID  22  at  which  time  periungual  and  generalized  des- 
quamation were  noted.  Serial  CBCs  showed  a persis- 
tant microcytic  anemia,  thrombocytopenia,  neutro- 
penia (the  absolute  neutrophil  count  was  less  than 
1,000  from  ID  17  to  ID  23),  and  lymphocytosis.  The 
reticulocyte  count  began  to  increase  on  ID  19.  Throm- 
bocytopenia resolved  on  ID  23.  The  maximum  platelet 
count  was  533,000  on  ID  26. 

A 2D  echocardiogram  on  ID  23  showed  large, 
diffuse,  sausage-shaped  coronary  artery  aneurysms 
with  a moderate  pericardial  effusion.  Aspirin  therapy 
was  started  at  10  mg/kg/day.  On  ID  29  the  ECG  showed 
Q waves  present  in  the  inferior  leads.  Serial  cardiac 
isoenzymes  were  negative.  A repeat  echocardiogram 
showed  some  dyskinesis  of  the  inferior  portion  of  the 
intraventricular  septum.  A multigated  acquisition  scan 
showed  a normal  ejection  fraction.  A thallium  scan 
showed  decreased  tracer  uptake  in  the  inferior  region 
of  the  heart.  After  the  resolution  of  the  pericardial 
effusion,  the  infant  was  discharged  to  the  care  of  his 
pediatrician.  As  of  this  writing,  he  is  doing  well. 

COMMENT 

The  CDC  defines  KS  as  an  illness  characterized 
by  unexplained  fever  for  longer  than  5 days  and  at 
least  four  of  the  following:  1)  bilateral  conjunctival 
injection;  2)  mucous  membrane  changes,  including 
injected,  dry  or  fissured  lips,  pharyngeal  injection  and 
strawberry  tongue;  3)  changes  in  the  extremities,  in- 
cluding erythema  of  the  palms  and  soles,  edema  of 
the  hands  or  feet,  and  generalized  or  periungual  des- 
quamation; 4)  rash;  5)  cervical  adenopathy.  Other 
commonly  reported  findings  include  sterile  pyuria,^'  ^ 
diarrhea,^'  ^ and  elevated  liver  enzymes.^'  ^ Approxi- 
mately 20%  of  all  cases  develop  aneurysms  of  the 
coronary  arteries.^-  ^ At  the  time  that  the  coronary  ar- 
tery aneurysms  are  discovered,  a thrombocytosis  and 
a polymorphonuclear  leukocytosis  are  seen.  This  is 
usually  during  the  second  or  third  week  of  the  illness.^ 

During  that  period  in  our  patient's  illness,  throm- 
bocytopenia and  neutropenia  were  observed.  A bone 

34  JOURNAL  VOL  140  JULY 


marrow  aspiration  showed  suppression  of  erythro- 
cyte and  granulocyte  precursors.  These  changes  have 
not  been  reported  with  KS.  They  are  seen  with  viral 
infection®'  ^ and  drug  allergy.  These  associations  made 
viral  infection  or  drug  allergy  the  most  probable  causes 
of  this  patient's  prolonged  illness. 

This  case  did,  however,  fulfill  the  CDC  clinical 
criteria  for  KS  even  before  the  echocardiogram  was 
obtained.  It  is  possible  that  more  than  one  pathologic 
process  occurred.  The  clinical  course  and  the  almost 
pathognomonic  findings  of  coronary  aneurysms  and 
infarct  make  a diagnosis  of  KS  unavoidable.  The  neu- 
tropenia and  thrombocytopenia  suggest  a second 
process  which,  in  this  case,  is  more  likely  due  to  drug 
allergy  than  a simultaneous  viral  infection.  The  pres- 
ence of  antibodies  to  platelets  and  granulocytes,  of 
depressed  complement  levels,  of  negative  viral  cul- 
tures, and  of  negative  serologic  studies  support  this 
conclusion. 

The  rapid,  presumptive  diagnosis  of  KS  consist- 
ent with  CDC  clinical  guidelines  is  important.  Treat- 
ment of  patients  with  KS  with  aspirin  and  intravenous 
immunoglobulin  within  10  days  of  the  onset  of  fever 
has  proven  to  be  effective  in  reducing  the  formation 
of  coronary  artery  aneurysms. This  patient  was  not 
found  to  have  aneurysms  until  ID  23  because  the  proc- 
ess of  making  a clinical  diagnosis  of  KS  was  con- 
founded by  the  drug  allergy  induced  hematologic 
findings.  By  then  the  therapeutic  window  was  closed. 
It  should  be  emphasized,  especially  because  timely 
therapy  is  effective  in  improving  outcome,  that  KS  is 
a clinical  diagnosis  and  that,  at  present,  laboratory 
findings  can  play  only  a supportive  role.  ■ 

REFERENCES 

1.  Kawasaki  T,  Kosaki  F,  Okgwa  S,  et  al:  A new  infantile  acute  febrile 
mucocutaneous  lymph  node  syndrome  prevailing  in  Japan.  Pediatrician 
1974;54:271-276. 

2.  Bell  DM,  Morens  DM,  Holman  R,  et  al:  Kawasaki  syndrome  in  the  United 
States.  Am  J Dis  Child  1983;137:211-214. 

3.  MeUsh  ME:  Kawasaki  syndrome:  A new  infectious  disease?  J Infect  Dis 
1981;143:317-324. 

4.  Morens  DM,  Anderson  L,  Hurwitz  E,  et  al:  National  surveillance  of 
Kawasaki  disease.  Pediatrics  1980;65:21-25. 

5.  Dean  AG,  Melish  M,  Hicks  R,  et  al:  An  epidemic  of  Kawasaki  syndrome 
in  Hawaii.  J Pediatr  1982;100:552-557. 

6.  Black  CA,  Bocchini  J,  Everist  J,  et  al:  Mucocutaneous  lymph  node  syn- 
drome in  north  Louisiana:  Review  of  15  cases.  South  Med  J 1983;76:290- 
295. 

7.  Nakano  H,  Saito  A,  Ueda  K,  et  al:  Clinical  characteristics  of  myocardial 
infarction  following  Kawasaki  disease:  Report  of  11  cases.  / Pediatr 
1986;108:198-203. 


8.  Blacklock  HA,  Mortimer  PP:  Aplastic  crisis  and  other  effects  of  human 
parvovirus  infection.  Clin  Haeeamatol  1984;13:679-691. 

9.  Yoimg  N,  Mortimer  P:  Viruses  and  bone  marrow  failure.  Blood  1984;63:729- 
737. 

10.  VanArsdel  PP  Jr:  Drug  allergy:  An  update.  Med  Clin  North  Am  1981;65:1089- 
1102. 

11.  Newburger  JW,  Takahashi  M,  Bums  JC,  et  al:  The  treatment  of  Kawasaki 
syndrome  with  intravenous  gamma  globulin.  N Engl  J Med  1986;315:341- 
347. 


Drs  Cohen  and  Whistler  are  from  the  Dept  of  Pediatrics  at  Tulane 
University  School  of  Medicine  in  New  Orleans. 

Reprints  will  not  be  available. 


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36 


JOURNAL  VOL  140  JULY 


CESAREAN  CHILDBIRTH  RATE 
AMONG  WOMEN  IN  THE 
NEW  ORLEANS  AREA 


JOAN  H.  WIGHTKIN,  MPH;  LINDA  M.  LAMBERT,  MPH 


The  national  rate  of  cesarean  section  delivery  more 
than  doubled  between  1975  and  1985,  from  10.4  to 
22.7.  In  1984,  when  the  US  cesarean  delivery  rate 
was  21.1  cesareans  per  100  deliveries,  a Southeast 
Louisiana  Health  Cost  Management,  Inc  study 
entitled  Medical  Cost  Utilization  Study,  1984 
showed  a cesarean  childbirth  rate  of  34.8  per  100 
deliveries  for  656  deliveries  in  the  New  Orleans 
metropolitan  area.  This  article  presents  the  results 
of  an  indepth  survey  of  the  cesarean  section  rates 
for  hospitals,  insurance  carriers,  Medicaid,  and 
Charity  Hospital  for  the  New  Orleans  area.  The 
1985  cesarean  rate  for  15  New  Orleans  area 
hospitals  including  Charity  Hospital  was  28.2  per 
100  deliveries,  which  was  higher  than  the  national 
(22.7)  and  southern  (23.5)  rate.  The  cesarean 
section  rate  for  insured  women  in  New  Orleans 
was  significantly  higher  than  that  for  the  Medicaid 
and  Charity  Hospital  population.  The  rate  of 
increase  in  cesarean  sections  in  the  New  Orleans 
area  is  also  examined.  This  article  outlines  the 
factors  contributing  to  the  increasing  cesarean 
delivery  rate  nationwide  and  calls  for  action  on  the 
part  of  the  medical  community. 


Physicians  from  the  Orleans,  Jefferson,  and  St  Bernard 
parish  medical  societies  provided  significant  input  into  the 
preparation  of  this  study.  Physicians  who  were  members  of 
Southeast  Louisiana  Health  Cost  Management's  Medicine! 
Industry  Task  Force,  as  well  as  guest  physicians,  analyzed 
all  of  the  extensive  data  and  informational  materials  collected 
in  order  to  report  the  facts  as  simply  as  possible.  The  fol- 
lowing report  was  reviewed  by  these  physicians  for  its  med- 
ical appropriateness  and  its  accuracy.  It  points  out  the  need 
for  further  study  to  determine  the  reasons  for  the  higher 
than  average  rate  of  cesarean  sections  in  New  Orleans. 

The  dramatic  increase  in  the  number  of  cesarean 
deliveries  performed  nationwide  over  the  past  15 
years  warrants  close  examination  by  providers,  con- 
sumers, and  payors  of  health  care. 

In  1975, 10.4  per  100  deliveries  in  the  United  States 
were  by  cesarean  childbirth.  By  1985,  that  figure  had 
more  than  doubled  to  22.7  (Table  1).^'  ^ That  year,  the 
southern  region  had  the  highest  rate  (23.5)  of  the  four 
regions  of  the  United  States. 

In  1984,  when  the  national  rate  was  21.1  cesar- 
eans per  100  deliveries,  a Southeast  Louisiana  Health  ► 

journal  VOL  140  JULY  39 


TABLE  1 

US  CESAREAN  DELIVERY  RATES  PER  100  DELIVERIES 


Cesarean 


Year 

Rate 

1970 

5.5 

1975 

10.4 

1980 

16.5 

1985 

22.7 

Source  of  data:  Taffel  SM,  Placek  PJ,  Liss  TL:  Trends  in  the 
United  States  cesarean  section  rate  and  reasons  for  the  1 980- 
1 985  rise.  Am  J Public  Health  1 987. 


Cost  Management  Inc  (SLHCM)  study  entitled  Med- 
ical Cost  Utilization  Study,  1984,  showed  a cesarean 
childbirth  rate  in  656  deliveries  at  34,8  for  the  New 
Orleans  metropolitan  area.  The  data  for  this  study 
were  medical  claims  from  13  employer  groups  and  a 
group  of  2,500  small  companies  who  insured  75,628 
people.  The  high  cost  and  the  frequency  of  this  sur- 
gical procedure  motivated  the  authors  to  look  further 
at  the  cesarean  childbirth  rate  by  gathering  more  sub- 
stantial data  and  presenting  them  in  this  report  to  the 
medical  community. 

METHOD 

A survey  was  mailed  to  21  New  Orleans  area  hos- 
pitals, the  Metropolitan  Hospital  Council  of  New  Or- 
leans, and  18  insurers,  third  party  administrators. 
Health  Maintenance  Organizations  (HMO),  and  Pre- 
ferred Provider  Organizations  (PPO).  The  informa- 
tion requested  on  the  survey  was:  the  total  number 
of  deliveries,  the  number  of  cesarean  deliveries,  the 
number  of  primary  cesarean  deliveries,  and  the  num- 
ber of  repeat  cesarean  deliveries  for  each  year  from 
1981  through  1986  in  the  New  Orleans  area.  The  sur- 
vey indicated  that  company/hospital  names  would  be 
kept  confidential  if  requested. 

The  Metropolitan  Hospital  Council  of  New  Or- 
leans provided  aggregate  data  for  14  area  hospitals 
covering  all  1985  admissions  together  with  a break- 
down of  births  by  age  of  the  mother,  payor  source, 
and  method  of  delivery.  Also,  six  hospitals  responded 
individually  to  the  survey.  Data  from  one  hospital 
were  not  used  because  the  data  covered  years  1981 

40  JOURNAL  VOL  140  JULY 


through  1983  only.  Four  hospitals  provided  primary 
and  repeat  cesarean  section  statistics.  One  HMO  and 
one  PPO  answered  the  survey.  Five  insurers  re- 
sponded to  the  survey.  In  addition,  data  were  ex- 
tracted from  a proprietary  insurance  data  base  which 
includes  a number  of  insurance  company  statistics. 
This  data  base  is  reported  as  Aggregate  Insurance 
Data  and  may  include  some  of  the  other  five  insurers 
responding  to  the  survey.  The  presentation  of  data  is 
limited  to  the  Metropolitan  Hospital  Council,  Charity 
Hospital,  four  individual  hospitals,  and  the  Aggregate 
Insurance  Data. 

RESULTS 

The  Metropolitan  Hospital  Council  of  New  Orleans' 
data  base  showed  a cesarean  section  rate  of  32.8  per 
100  deliveries  for  10,276  deliveries  with  3,367  cesarean 
sections  for  1985.  The  1985  rate  for  Charity  Hospital 
of  New  Orleans  was  20.4  per  100  deliveries  for  5,927 
deliveries  with  1,208  cesareans  performed.  For  the  14 
hospitals  included  in  the  Metropolitan  Hospital 
Council  data  base  plus  the  Charity  Hospital  of  New 
Orleans  data,  the  cesarean  section  rate  was  28.2  per 
100  deliveries.  The  true  cesarean  section  rate  lies  be- 
tween 27.5  per  100  and  28.9  per  100  with  a confidence 
of  97.5,  which  is  approximately  two  standard  devia- 
tions. This  was  based  on  16,203  deliveries  with  4,575 
cesarean  sections  and  represents  71.8%  of  all  births 
occurring  in  Orleans  and  Jefferson  parishes.  In  1985, 
the  New  Orleans  area  cesarean  section  rate  was  higher 
than  the  national  rate  and  higher  than  the  rate  for  the 
southern  region.  From  Table  2,  the  difference  can  also 
be  observed  when  the  Metropolitan  Hospital  Council 
data  are  broken  down  by  the  age  of  the  mother. 

The  New  Orleans  area  hospital  cesarean  delivery 
rates  as  reported  by  individual  hospitals  are  higher 
than  the  national  average  except  for  Charity  Hospital 
of  New  Orleans  (Fig  1).  The  average  annual  increase 
in  the  national  cesarean  section  rate  between  1981  and 
1986  was  1.2  percentage  points  per  year.  The  average 
increase  per  year  for  each  of  the  New  Orleans  hos- 
pitals reporting  data  for  1981  to  1986  was:  Hospital  1, 
2.0  percentage  points  per  year;  Hospital  2,  1.3  per- 
centage points  per  year;  Hospital  3,  2.3  percentage 
points  per  year.  The  cesarean  section  rate  for  Hospital 
4 increased  4.0  percentage  points  from  1985  to  1986. 
The  cesarean  section  rate  for  Charity  Hospital  of  New 
Orleans  decreased  0.5  percentage  points  from  1985  to 
1986. 


TABLE  2 

CESAREAN  SECTION  RATES  (PER  100  DELIVERIES)  FOR  NON-FEDERAL  SHORTSTAY  HOSPITALS 
FOR  THE  UNITED  STATES,  THE  SOUTH,  AND  THE  NEW  ORLEANS  AREA 


Metropolitan 

Hospital 

Charity 

Council  of 

Hospital 

United 

New  Orleans 

of  New 

States 

South 

Data* 

Orleans 

C-Section 
Rate  for 
the  New 
Orleans 
Areaf 


Total 

Age  of  Mother 
(Years) 

22.7 

23.5 

32.8 

(10,276) 

deliveries 

<20 

16.1 

16.0 

27.0 

20-24 

21.2 

22.6 

29.1 

25-29 

22.9 

23.4 

33.2 

30-34 

26.6 

30.7 

37.5 

35> 

30.7 

30.6 

43.8 

20.4 

(5,927) 

deliveries 


28.2 

(16,203) 

deliveries 


Source  of  data:  For  the  United  States  and  the  South:  Placek  PJ,  Taffel  S,  Moien  M;  Cesarean  rate  increase  in  1985.  Am  J Public  Health 
1987;77:241-242.  New  Orleans  rates:  Metropolitan  Hospital  Council  of  New  Orleans  and  Charity  Hospital  of  New  Orleans,  1985. 


‘Metropolitan  Hospital  Council  of  New  Orleans  Data  includes  1 4 area  hospitals  excluding  Charity  Hospital  of  New  Orleans. 

tCesarean  rate  for  New  Orleans  area  is  the  combined  Metropolitan  Hospital  Council  of  New  Orleans  data  and  Charity  Hospital  of  New 
Orleans  data. 


hospital  #4 

hospital  #3 

■ hospital  #2 

hospital  #1 

■Hi  USA 

Charity 

Hospital  at 
New  Orleans 

Source  of  data:  For  United  States:  Placek 
PJ,  Taffel  SM,  LissTL:  The  cesarean  future. 
American  Demographics  1987.  For  New 
Orleans:  Self-reported  by  five  New  Orleans 
hospitals. 


Fig  1.  Cesarean  delivery  rate  per  100  deliveries  for  the  United  States  and  five  New  Orleans  area  hospitals. 


JOURNAL  VOL  140  JULY  41 


TABLE  3 

CESAREAN  DELIVERY  RATES  FOR  A SEGMENT  OF  THE  INSURED  POPULATION  OF  NEW  ORLEANS 

AGGREGATE  INSURANCE  COMPANY  DATA 


Total 

Total 

40 

Year 

Rate 

Deliveries 

Cesarean 

1983 

27.6 

3128 

863 

38 

1984 

29.4 

6363 

1873 

36 

1985 

33.6 

8296 

2790 

1986 

38.8 

8267 

3210 

rate 

34 

per 

100 

deliveries 


32 


30 


28 


1 


1 


83  84  85  86 

years 


Source  of  data:  Aggregate  Insurance  Company  Data  for  the  New  Orleans  area,  1 987. 


TABLE  4 

CESAREAN  SECTION  RATE  BY  EXPECTED  SOURCE  OF  PAYMENT  FOR  THE  UNITED  STATES  AND  THE 
SOUTHERN  REGION  COMPARED  WITH  THE  CESAREAN  SECTION  RATE  FOR  8,495  DELIVERIES  IN 
FOURTEEN  NEW  ORLEANS  HOSPITALS  EXCLUSIVE  OF  CHARITY  HOSPITAL  OF  NEW  ORLEANS 


Medicaid Blue  Cross Other  Commercial  Insurance 


United 

States 

South 

New 

Orleans 

United 

States 

South 

New 

Orleans 

United 

States 

South 

New 

Orleans 

Total 

20.1 

19.4 

25.60-29.00* 

24.6 

24.2 

32.40-38.93* 

24.7 

27.1 

35.39-38.21* 

Age  of  Mother 
(years) 
<30 

18.9 

N/A 

27.1 

23.2 

N/A 

32.8 

23.0 

N/A 

33.7 

>30 

29.2 

N/A 

29.0 

27.5 

N/A 

40.0 

28.5 

N/A 

42.5 

Source  of  data:  National  and  southern  rates:  Tabulation  from  the  National  Center  for  Health  Statistics  from  National  Hospital  Discharge 
Survey,  1985.  New  Orleans  rates:  Metropolitan  Hospital  Council  of  New  Orleans  Data,  1985. 


‘The  true  rate  is  expected  to  tie  in  this  interval  with  a 97.5%  confidence. 


Primary  cesarean  section  rate  is  defined  as  the 
ratio  of  the  number  of  first  cesarean  sections  to  the 
number  of  mothers  who  never  had  a cesarean  section. 
The  primary  cesarean  section  rate  is  predictive  of  the 
rate  of  increase  in  the  overall  cesarean  section  rate 
because  subsequent  births  will  likely  be  sections.^  In 
1985,  the  primary  cesarean  section  rate  for  the  four 


New  Orleans  hospitals  with  4,132  deliveries  was  24,3 
compared  to  the  primary  cesarean  section  rate  for  the 
United  States  of  16.3.  The  true  primary  rate  for  New 
Orleans  hospitals  would  be  between  22.86  and  25.74 
with  a 97.5%  confidence,  which  is  approximately  two 
standard  deviations.  The  primary  rate  for  the  United 
States  increased  1.1  percentage  points  between  1985 


42  JOURNAL  VOL  140  JULY 


and  1986  to  17.4  while  the  primary  rate  for  the  four 
New  Orleans  hospitals  increased  2.8  percentage  points 
from  24.3  to  27.1.  The  true  primary  rate  for  the  four 
New  Orleans  hospitals  for  1986  was  between  25.74 
and  28.53  with  a confidence  of  97.5%,  which  is  ap- 
proximately two  standard  deviations. 

Aggregate  Insurance  Data  provided  a large  sample 
of  insured  deliveries  in  the  New  Orleans  area.  In  1986, 
there  were  8,267  deliveries  with  3,210  cesarean  deliv- 
eries yielding  a cesarean  delivery  rate  of  38.8  per  100 
deliveries  (Table  3).  The  national  cesarean  section  rate 
increased  3.8  percentage  points  from  20.3  in  1983  to 
24.1  in  1986.  In  the  Aggregate  Insurance  Data,  the 
cesarean  section  rate  increased  11.2  percentage  points 
between  1983  and  1986,  from  27.6  to  38.8. 

The  Metropolitan  Hospital  Council  of  New  Or- 
leans data  base  was  broken  down  by  expected  source 
of  payment  for  comparison  with  national  data.  The 
cesarean  section  rate  for  New  Orleans  was  statistically 
significantly  higher  than  the  rate  for  the  United  States 
and  the  South  in  three  payor  categories:  Medicaid, 
Blue  Cross,  and  Other  Commercial  Insurance  (Table 
4).  Among  Medicaid  patients,  the  rate  of  cesarean 
deliveries  was  statistically  significantly  lower  than  the 
rate  for  patients  covered  by  Blue  Cross  and  Other 
Commercial  Insurance  in  New  Orleans.  Similar  trends 
can  be  observed  when  the  data  is  broken  down  by 
the  age  of  the  mother,  with  the  greatest  difference 
occurring  between  the  United  States  rates  and  the 
rates  in  New  Orleans  for  Blue  Cross  and  for  Other 
Commercial  Insurance  Companies  (Table  4). 


Most 
patients 
need 
only  one. 


DISCUSSION 

This  study  demonstrates  that  the  cesarean  section  rate 
in  New  Orleans  exceeds  both  the  national  and  south- 
ern regional  rates.  The  cesarean  section  rate  for  the 
insured  patient  is  significantly  higher  than  that  for 
Medicaid  and  Charity  Hospital  patients.  Among  the 
four  hospitals  submitting  data  on  primary  cesarean 
sections,  the  primary  section  rate  significantly  ex- 
ceeded the  national  rate. 

The  medical  literature  points  to  the  following  fac- 
tors as  the  leading  contributors  to  the  increasing  ce- 
sarean childbirth  rate. 

• There  has  been  an  increase  in  the  diagnosis  of  dys- 
tocia and  fetal  distress  and  the  subsequent  use  of 
cesarean  section  as  intervention.^ 

• The  use  of  cesarean  delivery  for  breech  presentation 

has  increased  from  14.8%  in  1970  to  80.7%  in  1985. ^ ► 


Microburst 

Release 

System" 


(potassium  chloride)  20mEq 

A daily  prophylactic  dose 
in  a single  tablet. 

Please  see  next  page  for  brief  summary  of  prescribing  information. 


Pharmaceuticals,  Inc. 
Kenilworth,  NJ  07033 

World  leader  in  drug  delivery  systems. 


Copyright  © 1987,  Key  Pharmaceuticals,  Inc.,  Kenilworth,  NJ  07033. 
All  rights  reserved.  KD-2055/14238603H  8/87 


K->UH 

(potassium  chloride) 


Microburst 

Fielease 

System" 

Sustaned  Release  Tablets 


INDICATIONS  AND  USAGE;  BECAUSE  OF  REPORTS  OF  INTESTINAL  AND  GASTRIC  ULCERATION  AND 
BLEEDING  WITH  SLOW-RELEASE  POTASSIUM  CHLORIDE  PREPARATIONS,  THESE  DRUGS  SHOULD 
BE  RESERVED  FOR  THOSE  PATIENTS  WHO  CANNOT  TOLERATE  OR  REFUSE  TO  TAKE  LIQUID  OR  EF- 
FERVESCENT POTASSIUM  PREPARATIONS  OR  FOR  PATIENTS  IN  WHOM  THERE  IS  A PROBLEM  OF 
COMPLIANCE  WITH  THESE  PREPARATIONS. 

1.  For  therapeutic  use  in  patients  with  hypokalemia  with  or  without  metabolic  alkalosis,  in  digitalis 
intoxication  and  in  patients  with  hypokalemic  familial  periodic  paralysis. 

2.  For  the  prevention  of  potassium  depletion  when  the  dietary  intake  is  inadequate  in  the  following 
conditions:  Patients  receiving  digitalis  and  diuretics  for  congestive  heart  failure,  hepatic  cirrhosis 
with  ascites,  states  of  aldosterone  excess  with  normal  renal  function,  potassium-losing  nephropathy, 
and  with  certain  diarrheal  states. 

3.  The  use  of  potassium  salts  in  patients  receiving  diuretics  for  uncomplicated  essential  hyperten- 
sion is  often  unnecessary  when  such  patients  have  a normal  dietary  pattern.  Serum  potassium 
should  be  checked  periodically,  however,  and  if  hypokalemia  occurs,  dietary  supplementation  with 
potassium-containing  foods  may  be  adequate  to  control  milder  cases.  In  more  severe  cases  sup- 
plementation with  potassium  salts  may  be  indicated. 

CONTRAINDICATIONS:  Potassium  supplements  are  contraindicated  in  patients  with  hyperkalemia 
since  a further  increase  in  serum  potassium  concentration  in  such  patients  can  produce  cardiac 
arrest.  Hyperkalemia  may  complicate  any  of  the  following  conditions:  Chronic  renal  failure,  systemic 
acidosis  such  as  diabetic  acidosis,  acute  dehydration,  extensive  tissue  breakdown  as  in  severe  burns, 
adrenal  insufficiency,  or  the  administration  of  a potassium-sparing  diuretic  (e.g.,  spironolactone, 
triamterene). 

Wax-matrix  potassium  chloride  preparations  have  produced  esophageal  ulceration  in  certain  cardi- 
ac patients  with  esophageal  compression  due  to  enlarged  left  atrium. 

All  solid  dosage  forms  of  potassium  chloride  supplements  are  contraindicated  in  any  patient  in 
whom  there  is  cause  for  arrest  or  delay  in  tablet  passage  through  the  gastrointestinal  tract.  In  these 
instances,  potassium  supplementation  should  be  with  a liquid  preparation. 

WARNINGS;  Hyperkalemia— In  patients  with  impaired  mechanisms  for  excreting  potassium,  the  ad- 
ministration of  potassium  salts  can  produce  hyperkalemia  and  cardiac  arrest.  This  occurs  most  com- 
monly in  patients  given  potassium  by  the  intravenous  route  but  may  also  occur  in  patients  given 
potassium  orally.  Potentially  fatal  hyperkalemia  can  develop  rapidly  and  be  asymptomatic.  The  use  of 
potassium  salts  in  patients  with  chronic  renal  disease,  or  any  other  condition  which  impairs  potas- 
sium excretion,  requires  particularly  careful  monitoring  of  the  serum  potassium  concentration  and 
appropriate  dosage  adjustment. 

Interaction  with  Potassium  Sparing  Diuretics— Hypokalemia  should  not  be  treated  by  the  con- 
comitant administration  of  potassium  salts  and  a potassium-sparing  diuretic  (e.g.,  spironolactone  or 
triamterene)  since  the  simultaneous  administration  of  these  agents  can  produce  severe  hyperkalemia. 

Gastrointestinal  Lesions— Potassium  chloride  tablets  have  produced  stenotic  and/or  ulcerative 
lesions  of  the  small  bowel  and  deaths.  These  lesions  are  caused  by  a high  localized  concentration  of 
potassium  ion  in  the  region  of  a rapidly  dissolving  tablet,  which  injures  the  bowel  wall  and  thereby 
produces  obstruction,  hemorrhage  or  perforation, 

K-DUR  tabiets  contain  micro-crystalioids  which  disperse  upon  disintegration  of  the  tablet.  These 
micro-crystalloids  are  formulated  to  provide  a controlled  release  of  potassium  chloride.  The  dispersi- 
bility of  the  micro-crystalloids  and  the  controiled  release  of  ions  from  them  are  intended  to  minimize 
the  possibility  of  a high  local  concentration  near  the  gastrointestinal  mucosa  and  the  ability  of  the  KOI 
to  cause  stenosis  or  ulceration.  Other  means  of  accomplishing  this  (e.g.,  incorporation  of  potassium 
chloride  into  a wax  matrix)  have  reduced  the  frequency  of  such  lesions  to  less  than  one  per  100,000 
patient  years  (compared  to  40-50  per  100,000  patient  years  with  enteric-coated  potassium  chloride) 
but  have  not  eliminated  them.  The  frequency  of  Gl  lesions  with  K-DUR  tablets  is,  at  present, 
unknown.  K-DUR  tabiets  shouid  be  discontinued  immediately  and  the  possibility  of  bowel  obstruction 
or  perforation  considered  if  severe  vomiting,  abdominal  pain,  distention,  or  gastrointestinal  bleeding 
occurs. 

Metabolic  Acidosis— Hypokalemia  in  patients  with  metabolic  acidosis  should  be  treated  with  an 
alkalinizing  potassium  salt  such  as  potassium  bicarbonate,  potassium  citrate,  potassium  acetate,  or 
potassium  gluconate. 

PRECAUTIONS:  The  diagnosis  of  potassium  depletion  is  ordinarily  made  by  demonstrating  hypokale- 
mia in  a patient  with  a clinical  history  suggesting  some  cause  for  potassium  depletion.  In  interpreting 
the  serum  potassium  level,  the  physician  should  bear  in  mind  that  acute  alkalosis  per  se  can  produce 
hypokalemia  in  the  absence  of  a deficit  in  total  body  potassium  while  acute  acidosis  per  se  can  in- 
crease the  serum  potassium  concentration  into  the  normal  range  even  in  the  presence  of  a reduced 
total  body  potassium.  The  treatment  of  potassium  depletion,  particularly  in  the  presence  of  cardiac 
disease,  renal  disease,  or  acidosis  requires  careful  attention  to  acid-base  balance  and  appropriate 
monitoring  of  serum  electrolytes,  the  electrocardiogram,  and  the  clinical  status  of  the  patient. 

Laboratory  Tests:  Regular  serum  potassium  determinations  are  recommended.  In  addition,  during 
the  treatment  of  potassium  depletion,  careful  attention  should  be  paid  to  acid-base  balance,  other 
serum  electrolyte  levels,  the  electrocardiogram,  and  the  clinical  status  of  the  patient,  particularly  in 
the  presence  of  cardiac  disease,  renal  disease,  or  acidosis. 

Drug  Interactions:  Potassium-sparing  diuretics;  see  WARNINGS. 

Carcinogenesis,  Mutagenesis,  impairment  of  Fertility:  Long-term  carcinogenicity  studies  in 
animals  have  not  been  performed. 

Pregnancy  Category  C:  Animal  reproduction  studies  have  not  been  conducted  with  K-DUR.  It  is 
also  not  known  whether  K-DUR  can  cause  fetal  harm  when  administered  to  a pregnant  woman  or  can 
affect  reproduction  capacity.  K-DUR  should  be  given  to  a pregnant  woman  only  if  clearly  needed. 

Nursing  Mothers;  The  normal  potassium  ion  content  of  human  milk  is  about  13  mEq  per  liter.  Since 
oral  potassium  becomes  part  of  the  body  potassium  pool,  so  long  as  body  potassium  is  not  exces- 
sive, the  contribution  of  potassium  chloride  supplementation  should  have  little  or  no  effect  on  the 
level  in  human  milk. 

Pediatric  Use:  Safety  and  effectiveness  in  children  have  not  been  established. 

ADVERSE  REACTIONS:  One  of  the  most  severe  adverse  effects  is  hyperkalemia  (see  CONTRAINDICATIONS, 
WARNINGS,  and  OVERDOSAGE).  There  have  also  been  reports  of  upper  and  lower  gastrointestinal 
conditions  including  obstruction,  bleeding,  ulceration,  and  perforation  (see  CONTRAINDICATIONS 
and  WARNINGS);  other  factors  known  to  be  associated  with  such  conditions  were  present  in  many  of 
these  patients. 

The  most  common  adverse  reactions  to  oral  potassium  salts  are  nausea,  vomiting,  abdominal  dis- 
comfort, and  diarrhea.  These  symptoms  are  due  to  irritation  of  the  gastrointestinal  tract  and  are  best 
managed  by  taking  the  dose  with  meals  or  reducing  the  dose. 

Skin  rash  has  been  reported  rarely. 

OVERDOSAGE:  The  administration  of  oral  potassium  salts  to  persons  with  normal  excretory  mecha- 
nisms for  potassium  rarely  causes  serious  hyperkalemia.  However,  if  excretory  mechanisms  are  im- 
paired or  if  potassium  is  administered  too  rapidly  intravenously,  potentially  fatal  hyperkalemia  can 
result  (see  CONTRAINDICATIONS  and  WARNINGS).  It  is  important  to  recognize  that  hyperkalemia  is 
usually  asymptomatic  and  may  be  manifested  only  by  an  increased  serum  potassium  concentration 
and  characteristic  electrocardiographic  changes  (peaking  of  T-waves,  loss  of  P-waves,  depression  of 
S-T  segment,  and  prolongation  of  the  QT-interval).  Late  manifestations  include  muscle-paralysis  and 
cardiovascular  collapse  from  cardiac  arrest. 

Treatment  measures  for  hyperkalemia  include  the  following: 

1.  Elimination  of  foods  and  medications  containing  potassium  and  of  potassium-sparing  diuretics. 

2.  Intravenous  administration  of  300  to  500  ml/hr  of  10%  dextrose  solution  containing  10-20  units 
of  insulin  per  1,000  mi, 

3.  Correction  of  acidosis,  if  present,  with  intravenous  sodium  bicarbonate. 

4.  Use  of  exchange  resins,  hemodialysis,  or  peritoneal  dialysis. 

In  treating  hyperkalemia,  it  should  be  recalled  that  in  patients  who  have  been  stabiiized  on 
digitaiis,  too  rapid  a lowering  of  the  serum  potassium  concentration  can  produce  digitalis  toxicity. 

1002004 

Key  Pharmaceuticals,  Inc. 

Kenilworth,  NJ  07033  (USA) 

World  leader  in  drug  delivery  systems. 


13944326 
Rev.  4/87 


• There  is  continual  adherence  to  the  standard  “once 
a cesarean,  always  a cesarean,"  a phrase  originated 
in  1916  by  Dr  E.  B.  Craigin.  Of  women  with  pre- 
vious cesarean  deliveries  giving  birth  in  1985,  93% 
had  repeat  cesarean  deliveries.^ 

• The  fear  of  litigation  and  practice  of  defensive  med- 
icine is  a problem  in  obstetrics.  Before  1976,  mal- 
practice suits  were  filed  each  year  against  1 in  20 
obstetricians;  by  1985  that  proportion  had  increased 
to  1 in  6.^ 

The  New  Orleans  area  data  are  consistent  with  find- 
ings in  the  medical  literature  which  show  that  the 
insured  status  of  a patient  has  an  effect  on  cesarean 
delivery  rates. ^ In  1985,  the  New  Orleans  Medicaid 
population  had  a cesarean  section  rate  of  27.3  per  100 
deliveries  (2,726  Medicaid  deliveries)  and  the  Blue 
Cross  and  other  commercially  insured  New  Orleans 
area  population  had  a rate  of  36.5  per  100  deliveries 
(5,769  insured  deliveries).  The  difference  between  the 
cesarean  section  rate  for  Medicaid  and  insured  pa- 
tients was  4 percentage  points  in  the  national  data 
and  9 percentage  points  in  the  New  Orleans  data. 

The  medical  necessity  of  the  New  Orleans  area 
cesarean  delivery  rate  warrants  further  investigation. 
In  light  of  the  complex  medical,  legal,  and  insurance 
issues,  a multidisciplinary  committee  could  be  estab- 
lished to  develop  policy  recommendations  for  local 
hospitals,  providers,  and  consumers  with  respect  to 
the  local  cesarean  section  rate.  By  taking  a closer  look 
at  the  issues  surrounding  the  high  cesarean  rate  in 
New  Orleans,  the  medical  community  can  maintain 
its  position  of  leadership  and  its  protection  of  the 
standard  of  quality  of  care.  ■ 


REFERENCES 

1.  Taffel  S,  Placek  PJ,  Liss  TL;  Trends  in  the  United  States  cesarean  section 
rate  and  reasons  for  the  1980-85  rise.  Am  J Public  Health  1987;77:955-959. 

2.  Placek  PJ,  Taffel  S,  Moien  M:  Cesarean  rate  increase  in  1985.  Am  J Public 
Health  1987;77:241-242. 

3.  Shiono  PH,  Fielden  JC,  McNellis  D,  et  al:  Recent  trends  in  cesarean  birth 
and  trial  of  labor  rates  in  the  United  States.  JAMA  1987;257:494-497. 

4.  Casselberry  E:  Forum  on  malpractice  issues  in  childbirth.  Public  Health 
Rep  1985;100:629-633. 

5.  Placek  PJ,  Taffel  S.  Complications  in  cesarean  and  non-cesarean  deliveries: 
United  States,  1980.  Am  J Public  Health  1983;73:856-862. 


Ms  Wightkin  is  the  coordinator  of  the  Special  Supplemental  Food 
Program  for  Women  Infant  and  Children  (WIC)  for  the  Louisiana  Dept 


of  Health  £r  Hospitals.  Formerly  the  director  of  the  Louisiana  Maternal 
and  Child  Health  Program,  she  directed  the  nationally  recognized 
improved  Pregnancy  Outcome  Project.  Ms  Wightkin  is  a graduate  of 
Boston  University  and  Tulane  University  School  of 

Public  Health. 

Ms  Lambert  is  executive  director  of  Southeast  Louisiana  Health  Cost 
Management,  Inc.  Recognized  for  leadership  by  the  National  Council  on 
Family  Relations,  Ms  Lambert  is  a graduate  of  Louisiana  State 
University  and  the  University  of  North  Carolina  School  of 

Public  Health. 

Reprint  requests  should  be  sent  to  Linda  M.  Lambert,  Executive 
Director,  Southeast  Louisiana  Health  Cost  Management,  Inc, 
1440  Canal  St,  Suite  1704,  New  Orleans,  LA  70112. 

Acknowledgments  to  the  following  individuals,  who  contributed 
professional  expertise  to  this  project.  Medical  society  members:  Lynn 
Hickman,  MD;  Jay  Shames,  MD;  George  Ellis,  MD;  K.  Barton  Farris, 
MD;  Vincent  Culotta,  MD;  W’illiam  Renaudin,  MD;  Warren  Plauche, 
MD;  Frank  George,  MD;  Alarise  Gottlieb,  MD.  National  Center  for 
Health  Statistics:  Paul  Placek,  PhD;  Selma  Taffel;  Gregory  Pappas, 
MD,  PhD.  Industry  representatives:  Christfried  Unier.  MD;  Warren 
Perkins;  Erling  Hamjnarstrom;  G.  Edward  Woodmansee;  Carolyn 
Aides.  Aietropolitan  Hospital  Council  of  New  Orleans:  John  Finn,  PhD; 
Karin  Brown.  Charity  Hospital  at  New  Orleans:  Elliott  Roberts; 

Joseph  Aiiller,  MD. 


JOURNAL  VOL  140  JULY  45 


Re-introduce  The  Oldest 
Advance  In  Medicines. 


It’s  called  talking.  Right  or  wrong,  many  older  people  today 
feel  that  doctors  just  don’t  spend  as  much  time  talking 
with  their  patients  as  they  used  to.  Things  seem  more 
rushed  and  hurried. 

But  talking,  especially  about  medicines,  is  more  important 
than  ever  before.  Your  older  patients  may  be  taking  several 
different  medicines  and  seeing  more  than  one  doctor.  And 
many  older  people  are  treating  themselves  with  over-the- 
counter  drugs. 

Unfortunately,  an  older  person’s  response  to  medicines  is 
less  predictable  than  a younger  person’s.  They  can  experience 
altered  drug  actions  and  adverse  drug  reactions. 

So,  if  they  don’t  tell  you  first,  ask  them  what  they’re  taking 
and  if  the  medicines  are  causing  any  problems.  Take  a 
complete  medications  history  including  both  prescription 
and  non-prescription  medicines. 


Make  it  a point  to  tell  them  what  they  need  to  know  — the 
medicine’s  name,  how  and  when  to  take  it,  precautions,  and 
possible  side  effects.  Give  them  written  or  printed  information 
they  can  take  home,  and  encourage  them  to  write  down 
what  you  tell  them. 

Good,  clear  communication  about  medicines  can  increase 
compliance,  prevent  problems,  and  lead  to  better  health. 

So  re-introduce  the  oldest  advance  in  medicines.  Make 
talking  a crucial  part  of  your  practice.  It  isn’t  a thing  of  the 
past.  It’s  the  way  to  a healthier  future. 

Before  they  take  it, 
talk  about  it. 


^ National  Council  on 

Patient  Information  and  Education. 
666  Eleventh  St.  N.W.  Suite  810 
Washington,  D.C.  20001 


s 


PHYSICIAN 
SPECIALISTS. 


The  Air  Force  can  make  you  an  attractive 
offer — outstanding  compensation,  better 
working  hours  plus  opportunities  for 
professional  development.  You  con  hove 
o challenging  practice  and  time  to 
spend  with  your  family.  Find  out  what  the 
Air  Force  offers  a specialist  up  to  age  58. 
Call 

Capt  Frederick 
(817)  640-6469 

COLLECT 


Physicians  Recognition  Award 


Nineteen  physicians  from  the  state  of  Louisiana  were  awarded  the  Physicians  Recognition  Award  [PRA]  during 
April,  1988.  This  award  is  presented  by  the  American  Medical  Association  to  physicians  who  have  voluntarily 
completed  1 50  hours  of  continuing  medical  education  during  a consecutive  three-year  time  period.  Of  these  1 50 
hours,  at  least  60  must  be  in  AMA/PRA  Category  1 . These  nineteen  individuals  and  the  cities  in  which  they  reside 
are  presented  below. 


Bastrop 

James  Michael  Smith,  MD 


Jefferson 

Sandra  Kathleen  Mahkorn,  MD 


Baton  Rouge 

Henry  Raoul  Olivier,  MD 

Coushatta 

Fred  Spencer  Willis,  MD 

DeRidder 

John  Errol  McMillan,  MD 

Gretna 

Charles  Hunter  Watts,  MD 


Lafayette 

Stephen  Ira  Goldware,  MD 

Lake  Charles 

Clark  Alan  Gunderson,  MD 

Metairie 

Peter  Charles  Horowitz,  MD 


Houma 

Harold  Theodore  Conrad,  MD 


Monroe 

Alfred  Dent  Tisdale,  MD 


New  Orleans 

H.  Russell  Albright,  MD 
Robert  T.  Cook  III,  MD 

Opelousas 

Henry  E.  McLemore  II,  MD 
Michael  H.  Montgomery,  MD 

Ringgold 

Don  Gregory  Bell,  MD 

Shreveport 

Richard  Denman  Crow,  MD 
Edward  H.  Leatherman,  MD 
Baer  Irwin  Rambach,  MD 


All  recipients  are  members  of  the  Louisiana  State  Medical  Society. 


CALENDAR 


August 


August  13-14 

Anesthesia  for  the  Cardiac  Patient  Having  Non-Cardiac 
Surgery,  San  Diego.  Contact:  American  Society  of  Anesthe- 
siologists, 515  Basse  Hwy,  Park  Ridge,  IL  60068. 

Discussions  of  Current  Hand  Care  Concepts,  San  Diego. 
Contact:  Plastic  Surgery  Educational  Foundation,  444  East  Algon- 
quin Rd,  Arlington  Heights,  IL  60005;  (312)228-9900. 

August  14-19 

Wilderness  Medicine,  Snowmass,  Colorado.  Contact:  Office 
of  Continuing  Medical  Education,  UC  San  Diego  School  of 
Medicine,  M-017,  La  Jolla,  CA  92093-0617;  (619)534-3940. 

August  18-21 

Discussions  of  Current  Hand  Care  Concepts,  San  Diego. 
Contact:  Plastic  Surgery  Educational  Foundation,  444  East  Algon- 
quin Rd,  Arlington  Heights,  IL  60005;  (312)228-9900. 

August  21-30 

INTRAV  Cruise  on  the  Queen  Elizabeth  2 and  London,  Con- 
tact: Anita  Bums,  Louisiana  State  Medical  Society,  1700  Josephine 
St,  New  Orleans,  LA  70113;  (504)561-1033,  (800)462-9508. 

August  27 

Teleplast  Teleconference  on  Fasciocutaneous  Flaps, 

Metairie,  Shreveport,  and  Baton  Rouge,  Louisiana.  Contact: 
Plastic  Surgery  Educational  Foundation,  444  East  Algonquin  Rd, 
Arlington  Heights,  IL  60005;  (312)228-9900. 

September 


September  6-9 

3rd  Annual  Plastic  Surgery  of  the  Breast  Symposium,  San- 
ta Fe,  New  Mexico.  Contact:  Plastic  Surgery  Educational  Foun- 
dation, 444  East  Algonquin  Rd,  Arlington  Heights,  IL  60005; 
(312)228-9900. 

September  8-9 

Howto  Select  and  Evaluate  Residents,  Boston.  Contact:  The 
American  Board  of  Medical  Specialties,  PO  Box  1280,  Evanston, 
IL  60204;  (312)491-9091. 

September  10-18 

4th  Annual  Fall  Ultrasound  Symposia,  London  and  Paris. 
Contact:  Annual  Fall  Ultrasound  Meeting,  Medical  Seminars  In- 


ternational Inc,  21915  Roscoe  Blvd,  Suite  222,  Canoga  Park,  CA 
91304;  (818)719-7380. 

September  13-16 

39th  Annual  Conference  of  the  American  Group  Practice 
Association:  Charting  the  Course,  San  Diego.  Contact: 
AGP  A,  1422  Duke  St,  Alexandria,  VA  22314;  (703)838-0033. 

September  14-19 

Cosmetic  Surgery  of  the  Face  and  Breast,  Monte  Carlo, 
Monaco.  Contact:  Francine  Leinhardt,  Conference  Coordinator, 
210  East  64th  St,  New  York,  NY  10021;  (212)838-9200  ext  2776. 

September  17-18 

Metropolitan  Regional  Refresher  Course,  Las  Vegas.  Con- 
tact: American  Society  of  Anesthesiologists,  515  Basse  Hwy,  Park 
Ridge,  IL  60068. 

September  17-19 

4th  Annual  Meeting  of  the  American  Society  for  Reconstruc- 
tive Microsurgery,  Baltimore.  Contact:  ASRM,  3025  South 
Parker  Rd,  Suite  65,  Aurora,  CA  80014. 

September  29-30 

Issues  and  Concerns  Facing  IRBs  and  Clincial  Investigators, 

Austin,  Texas.  Contact:  Office  of  Continuing  Medical  Education, 
Scott  & White,  2401  South  31st  St,  Temple,  TX  76508; 
(817)774-2350. 


October 


October  3-5  | 

NIH  Consensus  Development  Conference:  Urinary  Incon-  | 
tinence  in  Adults,  Bethesda,  Maryland.  Contact:  Conference 
Registrar,  Prospect  Associates,  Suite  500,  1801  Rockville  Pike, 
Rockville,  MD  20852;  (30D468-MEET.  jj 

I 

October  3-7  j 

6th  Annual  Comprehensive  Review  of  Vascular  Siugery, 

Santa  Monica,  California.  Contact:  UCLA  Extension,